Ten Years of CRISPRing Cancers In Vitro

Article Oncology

Genome-wide CRISPR knockout screening identified G protein pathway suppressor 2 as a novel tumor suppressor for uveal melanoma metastasis

Shuangshuang Shi et al.

Summary: This study demonstrates that the GPS2 gene functions as a tumor suppressor in UM and may be a novel potential therapeutic target for UM treatment.

JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY (2023)

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Article Oncology

DCAF13 promotes breast cancer cell proliferation by ubiquitin inhibiting PERP expression

Bao-Qian Shan et al.

Summary: This study demonstrates that overexpression of DCAF13 is closely correlated with poor prognosis in human breast cancer. Knockdown of DCAF13 significantly reduces breast cancer cell proliferation, migration, and induces apoptosis, senescence, and cell cycle arrest. The study further reveals the interaction between DCAF13 and PERP, and the role of CRL4(DCAF13) E3 ligase in targeting PERP for degradation.

CANCER SCIENCE (2022)

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Article Biochemistry & Molecular Biology

Loss of SDHB Induces a Metabolic Switch in the hPheo1 Cell Line toward Enhanced OXPHOS

Mouna Tabebi et al.

Summary: This study suggests that mutations in the SDHB gene can lead to increased expression of GLUD1, which may serve as a potential biomarker and therapeutic target in SDHB mutated tumors.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2022)

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Article Oncology

Genome-wide CRISPR/Cas9 library screen identifies PCMT1 as a critical driver of ovarian cancer metastasis

Jingjing Zhang et al.

Summary: This study identified PCMT1 as a critical driver of resistance to detachment-induced apoptosis in ovarian cancer cells. PCMT1 enhanced cell migration, adhesion and spheroid formation through interaction with the ECM protein LAMB3. Treatment with an antibody against extracellular PCMT1 reduced cancer cell invasion and adhesion. PCMT1 was highly expressed in late-stage metastatic tumors, suggesting its potential as a therapeutic target in metastatic ovarian cancer.

JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH (2022)

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Article Biochemistry & Molecular Biology

Dual CRISPR interference and activation for targeted reactivation of X-linked endogenous FOXP3 in human breast cancer cells

Xuelian Cui et al.

Summary: This study proposes a potential therapy for female breast cancer by reactivating non-mutated allele and silencing XIST gene from X-chromosome inactivation. The simultaneous activation and repression of FOXP3 and XIST genes showed promising results in inhibiting tumor growth in vitro and in vivo.

MOLECULAR CANCER (2022)

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Article Biochemistry & Molecular Biology

Identifying novel therapeutic targets in gastric cancer using genome-wide CRISPR-Cas9 screening

Zhi Zeng et al.

Summary: This study identified 184 novel essential genes in gastric cancer cells using genome-wide CRISPR-Cas9 screening, and validated METTL1 as a potential therapeutic target for gastric cancer.

ONCOGENE (2022)

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Article Oncology

ELOVL2 promotes cancer progression by inhibiting cell apoptosis in renal cell carcinoma

Ken Tanaka et al.

Summary: This study found that ELOVL2 was highly expressed in ccRCC, pRCC, and chRCC, and its high expression was significantly associated with a poor prognosis. Knockdown of ELOVL2 suppressed the elongation of fatty acids, increased lipid droplet production, and inhibited tumor growth. These findings provide new insights into the tumor proliferation mechanisms involving lipid metabolism and suggest ELOVL2 as a potential novel target for RCC therapy.

ONCOLOGY REPORTS (2022)

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Article Cell Biology

Genome wide CRISPR/Cas9 screen identifies the coagulation factor IX (F9) as a regulator of senescence

Paula Carpintero-Fernandez et al.

Summary: In this study, a functional genome-wide CRISPR/Cas9 genetic screen was used to identify key genes involved in the proliferation arrest induced by CDK4/6 inhibitors. Downregulation of coagulation factor IX (F9) was found to prevent cell cycle arrest and senescent-like phenotype in breast tumor cells treated with Palbociclib. These findings can contribute to the design of new therapeutic strategies in personalized medicine to increase treatment efficiency, stratify patients, and overcome drug resistance.

CELL DEATH & DISEASE (2022)

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Review Oncology

Hallmarks of Cancer: New Dimensions

Douglas Hanahan

Summary: The concept of the hallmarks of cancer is a tool for simplifying the complexity of cancer phenotypes and genotypes into basic principles. This article proposes phenotypic plasticity and disrupted differentiation as distinct hallmark capabilities, and discusses nonmutational epigenetic reprogramming and polymorphic microbiomes as enabling characteristics. Additionally, the importance of senescent cells in the tumor microenvironment is highlighted. The integrative concept of the hallmarks of cancer helps in understanding the mechanisms of cancer development and applying that knowledge to cancer medicine.

CANCER DISCOVERY (2022)

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Article Oncology

Urokinase Receptor uPAR Downregulation in Neuroblastoma Leads to Dormancy, Chemoresistance and Metastasis

Anna A. Shmakova et al.

Summary: The expression of uPAR in neuroblastoma is associated with patient survival. High uPAR expression predicts poor survival, while relapsed neuroblastomas show significantly decreased uPAR expression. Downregulation of uPAR in neuroblastoma cells leads to dormancy and resistance to chemotherapy.

CANCERS (2022)

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Article Multidisciplinary Sciences

Article An inducible CRISPR/Cas9 screen identifies DTX2 as a transcriptional regulator of human telomerase

Zhifen Zhou et al.

Summary: This study identified multiple positive regulators, including the E3 ligase DTX2, through an inducible CRISPR/Cas9 KO screen. Depletion of DTX2 in telomerase-positive cancer cells resulted in downregulation of hTERT transcription and telomerase activity, leading to progressive telomere shortening, growth arrest, and increased apoptosis. BioID analysis revealed that DTX2 interacts with multiple transcription factors, with NFIC functioning cooperatively with DTX2 to promote hTERT transcription. Further investigation demonstrated that DTX2 mediates K63-linked ubiquitination of NFIC, which enhances NFIC binding to the hTERT promoter and increases hTERT expression.

ISCIENCE (2022)

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Article Oncology

OLA1 promotes colorectal cancer tumorigenesis by activation of HIF1α/CA9 axis

Yue Liu et al.

Summary: The study found that OLA1 was highly expressed in CRC and was associated with lower survival rate and poor prognosis. Knocking out OLA1 gene inhibited the growth and tumorigenesis ability of CRC cells. Further analysis revealed that the expression levels of hypoxic-related genes HIF1 alpha/CA9 were significantly downregulated after OLA1 knockdown, which may explain the impaired tumorigenesis. Additionally, OLA1 knockout resulted in over-activation of GSK3 beta. Therefore, OLA1 may contribute to the occurrence and prognosis of CRC through the activation of HIF1 alpha/CA9 axis and GSK3 beta.

BMC CANCER (2022)

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Article Oncology

Transcriptional Repression by FoxM1 Suppresses Tumor Differentiation and Promotes Metastasis of Breast Cancer

Dragana Kopanja et al.

Summary: This study provides new insights into the critical role of the interaction between FoxM1 and Rb in the plasticity and metastasis of breast cancer cells.

CANCER RESEARCH (2022)

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Article Cell Biology

ISL2 is a putative tumor suppressor whose epigenetic silencing reprograms the metabolism of pancreatic cancer

Harun Ozturk et al.

Summary: This study identifies ISL2 as a putative tumor suppressor in pancreatic ductal adenocarcinoma (PDA). ISL2 is epigenetically silenced and its reduced expression correlates with poor patient survival. ISL2 regulates the expression of metabolic genes and its depletion increases oxidative phosphorylation (OXPHOS). Spatial transcriptomic analysis shows heterogeneous intratumoral ISL2 expression, which correlates with the expression of critical metabolic genes.

DEVELOPMENTAL CELL (2022)

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Article Cell Biology

CRISPR-Cas9 screen identifies oxidative phosphorylation as essential for cancer cell survival at low extracellular pH

Johanna Michl et al.

Summary: Unlike most cell types, cancer cells can survive in low acid environments. Knocking out genes associated with pH-related fitness defects in colorectal cancer cells can cause cell death under acidic conditions. Researchers have also discovered mitochondrial metabolism inhibitors that can specifically kill cancer cells in a low acid environment. The growth of xenografts established from gene-knockout cells is slower, but can be stimulated with bicarbonate therapy to reduce tumor acid stress.

CELL REPORTS (2022)

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Article Biochemistry & Molecular Biology

CRISPR-mediated knockout of VEGFR2/KDR inhibits cell growth in a squamous thyroid cancer cell line

Ming-Lin Tsai et al.

Summary: The overexpression of VEGFC and VEGFR2/KDR in thyroid cancers suggest that the VEGF/VEGFR signaling pathway plays a carcinogenic role in cancer development. The selective targeting of KDR may have the potential to be a novel anti-cancer therapy.

FEBS OPEN BIO (2022)

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Article Chemistry, Multidisciplinary

CRISPR/Cas9 Screens Reveal that Hexokinase 2 Enhances Cancer Stemness and Tumorigenicity by Activating the ACSL4-Fatty Acid β-Oxidation Pathway

Hongquan Li et al.

Summary: This study identifies metabolic genes associated with liver cancer and stem cell properties using in vivo CRISPR/Cas9 screening. Among them, HK2 plays a key role in the maintenance and self-renewal of liver cancer stem cells. Blocking HK2 effectively inhibits liver cancer growth, suggesting a promising therapeutic strategy for liver cancer treatment.

ADVANCED SCIENCE (2022)

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Review Immunology

Effect of CRISPR/Cas9-Edited PD-1/PD-L1 on Tumor Immunity and Immunotherapy

Yanxin Xu et al.

Summary: This article summarizes the application and potential of CRISPR/Cas9 gene editing technology in tumor immunotherapy, as well as its importance in exploring tumor immune regulation mechanisms and clinical practice.

FRONTIERS IN IMMUNOLOGY (2022)

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Article Oncology

RB1-Negative Retinal Organoids Display Proliferation of Cone Photoreceptors and Loss of Retinal Differentiation

Deniz Kanber et al.

Summary: Retinoblastoma is a tumor of the retina that mainly affects children. It is caused by inactivation of the RB1 gene in retinal cells. This study aimed to establish a human laboratory model for retinoblastoma. By differentiating stem cells with a mutation in RB1 into the retina, the researchers observed similar characteristics to tumor development, such as reduced differentiation potential and enhanced proliferation. The gene expression in the model resembled that of tumor material. This model allows for research and potential therapy for retinoblastoma in the human retina.

CANCERS (2022)

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Article Oncology

Sphingomyelin Phodiesterase Acid-Like 3A Promotes Hepatocellular Carcinoma Growth Through the Enhancer of Rudimentary Homolog

Yu Zhang et al.

Summary: High expression of SMPDL3A in HCC was associated with poor prognosis. Knockout of SMPDL3A inhibited cell proliferation and migration in HCC cells. SMPDL3A interacted with ERH to affect the tumorigenesis and progression of HCC.

FRONTIERS IN ONCOLOGY (2022)

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Article Biochemical Research Methods

CRISPR/Cas9-mediated LINC00511 knockout strategies, increased apoptosis of breast cancer cells via suppressing antiapoptotic genes

Narjes Azadbakht et al.

Summary: This study utilized genetic knockout techniques to investigate the impact of LINC00511 gene deletion in breast cancer cells. Meta-analysis results showed that higher LINC00511 expression is associated with lower overall survival and increased lymph node metastasis. Functional experiments confirmed that LINC00511 promotes breast cancer cell proliferation and tumor growth. Additionally, the study found that the transcription factor E2F1 binds to the Nanog gene's promoter site to induce transcription.

BIOLOGICAL PROCEDURES ONLINE (2022)

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Article Biochemistry & Molecular Biology

ATF2 loss promotes tumor invasion in colorectal cancer cells via upregulation of cancer driver TROP2

Kerstin Huebner et al.

Summary: In colorectal cancer, low levels of ATF2 are associated with worse prognosis and tumor aggressiveness. TROP2 is identified as a novel inhibitory target gene of ATF2. In vitro studies demonstrated that high levels of TROP2 are critical for cell de-adhesion and increased cell migration. In vivo experiments confirmed that ATF2(KO)/TROP2(high) status promotes tumor invasiveness. Evaluation of ATF2(low)/TROP2(high) expression status may help identify high-risk CRC patients.

CELLULAR AND MOLECULAR LIFE SCIENCES (2022)

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Article Oncology

The SKP2-p27 axis defines susceptibility to cell death upon CHK1 inhibition

Michael Lohmueller et al.

Summary: Besides p53 status, the expression levels of SKP2 and p27 may also be important factors in predicting the responsiveness of cancer cells to CHK1 inhibitors.

MOLECULAR ONCOLOGY (2022)

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Review Biotechnology & Applied Microbiology

Macrophages as tools and targets in cancer therapy

Alberto Mantovani et al.

Summary: This review discusses the molecular mechanisms of macrophage reprogramming in the tumor microenvironment and provides an overview of macrophage-targeted therapies for cancer treatment.

NATURE REVIEWS DRUG DISCOVERY (2022)

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Article Cell Biology

EPIKOL, a chromatin-focused CRISPR/Cas9-based screening platform, to identify cancer-specific epigenetic vulnerabilities

Ozlem Yedier-Bayram et al.

Summary: This study generated an epigenome-wide CRISPR-Cas9 knockout library (EPIKOL) to investigate the roles of epigenetic modifiers in cancer cells. Through eight screens in different cancer types, novel epigenetic modifiers regulating TNBC and prostate cancer cell fitness were identified. The results demonstrate that EPIKOL can be used to identify essential epigenetic modifiers and discover novel anti-cancer targets.

CELL DEATH & DISEASE (2022)

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Article Cell Biology

Glycosphingolipids are mediators of cancer plasticity through independent signaling pathways

Cecile Cumin et al.

Summary: The molecular repertoire promoting cancer cell plasticity remains partly unknown, but this study proposes that glyco-sphingolipids, specifically globo and ganglio series, play a role in promoting the transition between epithelial and mesenchymal cells. The study found elevated levels of globosides in tumor compartments compared to the ganglioside-rich stroma. It also discovered that the ganglioside-synthesizing enzyme ST8SIA1 was consistently elevated in mesenchymal-like samples, indicating a poor outcome.

CELL REPORTS (2022)

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Article Physiology

Antagonizing Sec62 function in intracellular Ca2+ homeostasis represents a novel therapeutic strategy for head and neck cancer

Sandrina Koerner et al.

Summary: SEC62 gene amplification is frequently observed in various cancer types and is associated with poor outcomes and increased metastatic burden.Due to its intracellular localization, functional knockdown of SEC62 represents a promising approach for targeted therapy. Inhibition of SEC62 function can limit tumor growth and metastasis formation by increasing cellular stress levels.

FRONTIERS IN PHYSIOLOGY (2022)

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Article Oncology

ZNF677 suppresses renal cell carcinoma progression through N6-methyladenosine and transcriptional repression of CDKN3

Aolin Li et al.

Summary: ZNF677 functions as a tumor suppressor in RCC and its low expression is associated with unfavorable prognosis and decreased m(6)A modification level. Furthermore, m(6)A modification regulates the translation and mRNA stability of ZNF677.

CLINICAL AND TRANSLATIONAL MEDICINE (2022)

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Article Oncology

Genome-wide CRISPR/Cas9 screening for therapeutic targets in NSCLC carrying wild-type TP53 and receptor tyrosine kinase genes

Qianqian Wang et al.

Summary: This study identified MDM2 as a potential therapeutic target for wtTP53-RTK non-small cell lung cancer through genome-wide CRISPR/Cas9 screening. Treatment with MDM2 inhibitor RG7388 alone or in combination with pemetrexed resulted in significant tumor inhibition in this subgroup of patients.

CLINICAL AND TRANSLATIONAL MEDICINE (2022)

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Review Biochemistry & Molecular Biology

Epigenetic and Transcriptional Signaling in Ewing Sarcoma-Disease Etiology and Therapeutic Opportunities

Mingli Li et al.

Summary: This review discusses the epigenetic and transcriptional alterations in Ewing sarcoma and summarizes the relevant screening studies conducted to develop novel therapies.

BIOMEDICINES (2022)

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Article Cell Biology

CD95 gene deletion may reduce clonogenic growth and invasiveness of human glioblastoma cells in a CD95 ligand-independent manner

Clara Quijano-Rubio et al.

Summary: This study found that canonical CD95L may not be expressed in human glioma-initiating cells (GIC) but there exists a CD95L-independent CD95 signaling pathway that maintains malignant traits of the cells. The findings highlight the complexity and challenges associated with targeting CD95 for therapeutic purposes.

CELL DEATH DISCOVERY (2022)

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Article Biochemistry & Molecular Biology

Targeted demethylation at ZNF154 promotor upregulates ZNF154 expression and inhibits the proliferation and migration of Esophageal Squamous Carcinoma cells

Wenting He et al.

Summary: Zinc finger protein 154 (ZNF154) is hypermethylated at the promoter in esophageal squamous carcinoma (ESCC), leading to downregulation of the tumor suppressor gene and promoting cell proliferation and migration. Epigenetic editing using CRISPR/dCas9 technology can reverse the hypermethylation and inhibit ESCC cells. Furthermore, ZNF154 acts as a transcription factor to upregulate the expression of ESCC-associated tumor suppressor genes.

ONCOGENE (2022)

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Article Medicine, Research & Experimental

DNA promoter hypermethylation of melanocyte lineage genes determines melanoma phenotype

Adriana Sanna et al.

Summary: Cellular stress contributes to the phenotype switching of melanoma cells, and this is associated with the loss of specific gene expression and increased expression of mesenchymal markers. The loss of microphthalmia-associated transcription factor (MITF) and SRY-box transcription factor 10 (SOX10) is related to this process, and their loss is associated with promoter hypermethylation and poor patient survival.

JCI INSIGHT (2022)

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Review Oncology

Cellular and molecular mechanisms of plasticity in cancer

Stefan R. Torborg et al.

Summary: Cancer cells have plasticity and can rapidly adapt to their environment and evade therapy. This article provides an overview of the fundamental mechanisms underlying cancer cell plasticity, and highlights the crucial role of high-plasticity cell states in cell state transitions and intra-tumoral heterogeneity.

TRENDS IN CANCER (2022)

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Article Oncology

CRISPR/Cas9-mediated knockout of HO-1 decreased the proliferation and migration of T47D cells and increased cisplatin-induced apoptosis: an in vitro study

Sahar Evazi Bakhshi et al.

Summary: In this study, the CRISPR/Cas9 technology was used to knock out the HO-1 gene in breast cancer cells, and its effects on cell proliferation, cisplatin sensitivity, apoptosis, and migration capability were studied. The results revealed that suppression of HO-1 significantly inhibited cell proliferation, increased sensitivity to cisplatin-induced toxicity and apoptosis, and abolished cell migration capability.

MEDICAL ONCOLOGY (2022)

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Article Oncology

Polo-Like Kinase 1 Regulates Chromosomal Instability and Paclitaxel Resistance in Breast Cancer Cells

Mingji Quan et al.

Summary: PLK1 plays an important role in regulating genetic heterogeneity and taxane resistance in breast cancer. Silencing PLK1 can inhibit proliferation and enhance sensitivity to taxanes in breast cancer cells. Furthermore, PLK1 expression is associated with overall patient survival in breast cancer.

JOURNAL OF BREAST CANCER (2022)

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Article Oncology

Beta 2 adrenergic receptor and mu opioid receptor interact to potentiate the aggressiveness of human breast cancer cell by activating the glycogen synthase kinase 3 signaling

Benedicte Rousseau et al.

Summary: This study demonstrates that the interaction between opioid and beta-adrenergic receptors plays a role in controlling the growth and proliferation of triple-negative breast cancer cells. The inhibition of these receptors leads to a less aggressive phenotype in vitro and in vivo. The glycogen synthase kinase 3 (GSK3) pathway is potentially involved in mediating this cross talk between the receptors.

BREAST CANCER RESEARCH (2022)

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Article Biochemistry & Molecular Biology

Identification of NOXA as a pivotal regulator of resistance to CAR T-cell therapy in B-cell malignancies

Xin Yan et al.

Summary: Loss of NOXA, a BCL2 family protein, was identified as a key regulator of resistance to CAR T-cell therapy. Low NOXA expression was associated with worse survival in patients with B-cell lymphoma. In vitro and in vivo experiments showed that enhancing NOXA expression using HDAC inhibitors dramatically increased sensitivity of cancer cells to CAR T-cell clearance.

SIGNAL TRANSDUCTION AND TARGETED THERAPY (2022)

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Article Medicine, Research & Experimental

Epigenomic reprogramming via HRP2-MINA dictates response to proteasome inhibitors in multiple myeloma with t(4;14) translocation

Jingjing Wang et al.

Summary: The t(4;14) chromosomal translocation drives high expression of NSD2 and plays important roles in MM evolution and progression. HRP2 downregulation is associated with poor response and worse outcomes in PIs treatment, and its suppression promotes cell survival and restricts ER stress by increasing H3K27me3 levels.

JOURNAL OF CLINICAL INVESTIGATION (2022)

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Article Oncology

Dual inhibition of anti-apoptotic proteins BCL-XL and MCL-1 enhances cytotoxicity of Nasopharyngeal carcinoma cells

Siti Fairus Abdul Rahman et al.

Summary: Co-inhibition of BCL-XL and MCL-1/BFL-1 could be a potential treatment strategy for nasopharyngeal carcinoma.

DISCOVER ONCOLOGY (2022)

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Review Biochemistry & Molecular Biology

CRISPR/Cas9 in cancer therapy: A review with a special focus on tumor angiogenesis

Krishnasamy naidu gopal Hariprabu et al.

Summary: Tumor angiogenesis is a critical target for cancer treatment, but current anti-angiogenic medicines are ineffective due to compensatory molecular mechanisms. The development of gene-editing technology like CRISPR/Cas9 provides new possibilities for cancer therapy by dissecting carcinogenesis pathways, identifying new biological targets, and potentially arming cancer cells.

INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES (2021)

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Article Multidisciplinary Sciences

SHP2 blockade enhances anti-tumor immunity via tumor cell intrinsic and extrinsic mechanisms

Ye Wang et al.

Summary: The study unveiled a new immune modulatory function of SHP2, with inhibition promoting anti-tumor immunity by enhancing T cell cytotoxicity and immune-mediated tumor regression. Additionally, SHP2 inhibition improved responses to anti-PD-1 blockade, suggesting its potential as a promising strategy for cancer immunotherapy.

SCIENTIFIC REPORTS (2021)

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Article Oncology

Integrated Omics Analysis of Non-Small-Cell Lung Cancer Cells Harboring the EGFR C797S Mutation Reveals the Potential of AXL as a Novel Therapeutic Target in TKI-Resistant Lung Cancer

Tong-Hong Wang et al.

Summary: This study utilized CRISPR/Cas9 technology to introduce the EGFR C797S mutation into an NSCLC cell line, revealing an association between differentially expressed genes/proteins and increased AXL expression in cells with the mutation. Inhibition of AXL showed effectiveness in slowing the growth of NSCLC cells carrying EGFR C797S, suggesting it could be a potential treatment strategy for this type of TKI resistance.

CANCERS (2021)

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Review Biochemistry & Molecular Biology

Application of the CRISPR/Cas9-based gene editing technique in basic research, diagnosis, and therapy of cancer

Huimin Zhang et al.

Summary: The 2020 Nobel Prize in Chemistry was awarded to Emmanuelle Charpentier and Jennifer Doudna for their development of CRISPR/Cas9 gene editing technology, which has provided new tools for precise gene editing. This technology has been shown to be increasingly used in cancer research and treatment, achieving remarkable results in exploring tumorigenesis and development mechanisms.

MOLECULAR CANCER (2021)

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Article Genetics & Heredity

AKT-dependent signaling of extracellular cues through telomeres impact on tumorigenesis

Raul Sanchez-Vazquez et al.

Summary: This study demonstrates how extracellular signals can regulate telomere protection and length through modifications in TRF1 protein. Mutations in TRF1 lead to decreased telomere binding, increased DNA damage, accelerated telomere shortening, impaired response to proliferative signals, and decreased tumorigenesis potential. It highlights the role of PI3K/AKT pathway in regulating telomere maintenance and suggests potential targets for cancer therapy.

PLOS GENETICS (2021)

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Article Biochemistry & Molecular Biology

CRISPR-based knock-in mutagenesis of the pioneer transcription factor FOXA1: optimization of strategies for multi-allelic proteins in cancer cells

Shen Li et al.

Summary: The CRISPR-Cas9 technology has revolutionized precise genome engineering in living cells, facilitating research into human health and the discovery of novel therapeutics. While most widely used for inactivating or knocking out specific genes, it can also introduce subtle DNA sequence substitutions. Editing cancer cells with unstable genomes and multiple chromosomes is challenging, requiring optimized methodologies and experimental design. The successful editing of specific amino acids in FOXA1 protein in MCF-7 breast cancer cells using CRISPR-Cas9 highlights the potential for systematic analysis of molecular mechanisms in the appropriate physiological context.

FEBS OPEN BIO (2021)

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Article Multidisciplinary Sciences

Functional antagonism of chromatin modulators regulates epithelial-mesenchymal transition

Michela Serresi et al.

Summary: Research has shown that chromatin regulators have a broader impact on EMT interconversion in lung cancer cells than kinases, and the loss of ARID1A, DOT1L, BRD2, and ZMYND8 may have nondeterministic and sometimes opposite consequences. These findings reveal general principles underlying transcriptional control of cancer cell plasticity.

SCIENCE ADVANCES (2021)

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Article Oncology

Epigenome screening highlights that JMJD6 confers an epigenetic vulnerability and mediates sunitinib sensitivity in renal cell carcinoma

Chuanjie Zhang et al.

Summary: Aberrant epigenetic reprogramming is a hallmark of renal cell carcinoma (RCC) tumorigenesis. This study identified JMJD6 as a potent target in RCC, with its overexpression correlating with poor survival outcomes and promoting RCC progression. Targeting JMJD6 could suppress its oncogenic effects and sensitize RCC to sunitinib, showing synergistic effects when combined.

CLINICAL AND TRANSLATIONAL MEDICINE (2021)

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Article Medicine, Research & Experimental

CRISPR screens identify tumor-promoting genes conferring melanoma cell plasticity and resistance

Arthur Gautron et al.

Summary: Genetic drivers of melanoma development and therapy resistance have been identified, but non-genetic mechanisms are less understood. Through in vivo CRISPR screens, SMAD3, BIRC3, and SLC9A5 were found to play key roles in BRAFi resistance. Upregulation of SMAD3 was linked to resistance prediction and chemical inhibition of SMAD3 showed promise in targeting persister cells associated with melanoma.

EMBO MOLECULAR MEDICINE (2021)

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Article Health Care Sciences & Services

Knockout of Hepatocyte Growth Factor by CRISPR/Cas9 System Induces Apoptosis in Hepatocellular Carcinoma Cells

Han Ki Lee et al.

Summary: The CRISPR/Cas9 system utilizes noncoding RNAs to guide the Cas9 nuclease for site-specific DNA cleavage, while HGF is a crucial growth factor that promotes HCC cell growth. Inhibiting HGF via Crispr-HGF transfection can suppress cell proliferation and induce apoptosis in HCC cells.

JOURNAL OF PERSONALIZED MEDICINE (2021)

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Article Chemistry, Multidisciplinary

Programmable Unlocking Nano-Matryoshka-CRISPR Precisely Reverses Immunosuppression to Unleash Cascade Amplified Adaptive Immune Response

Jin Yang et al.

Summary: The PUN system targets PD-L1 and PTPN2 for permanent, complete and highly responsive immunotherapy. By releasing CRISPR/Cas9 to efficiently disrupt PD-L1 and PTPN2 in tumor cells, it enhances adaptive immune responses.

ADVANCED SCIENCE (2021)

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Article Oncology

Isochorismatase domain-containing protein 1 (ISOC1) participates in DNA damage repair and inflammation-related pathways to promote lung cancer development

Jinghan Shi et al.

Summary: The novel molecular target ISOC1 is upregulated in lung cancer, associated with poor disease-free survival. Overexpression of ISOC1 enhances proliferation, viability, migration, and invasion of NSCLC cells, while intronic miR-4633 also promotes tumor cell progression. Knockout of ISOC1 significantly inhibits tumor growth in vivo, demonstrating its potential as a therapeutic target for lung cancer.

TRANSLATIONAL LUNG CANCER RESEARCH (2021)

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Article Biotechnology & Applied Microbiology

CRISPR/Cas9-mediated activation of CDH1 suppresses metastasis of breast cancer in rats

Fatma Al-Mulhim et al.

Summary: This study demonstrated that knockout of CDK11 and activation of CDH1 using CRISPR/Cas9 technology can effectively inhibit cell cycle progression and reduce tumor cell infiltration. These findings suggest that CRISPR/Cas9 may be a promising approach for treating breast cancer.

ELECTRONIC JOURNAL OF BIOTECHNOLOGY (2021)

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Article Oncology

Identification of Autophagy-Related Genes as Targets for Senescence Induction Using a Customizable CRISPR-Based Suicide Switch Screen

Arnout Schepers et al.

Summary: Pro-senescence therapies are being considered for cancer treatment, with the challenge of identifying additional targets to induce senescence in cancer cells. A suicide switch system is presented for genome-wide CRISPR screening in growth-arrested subpopulations by eliminating proliferating cells. Autophagy-related proteins are identified as targets for senescence induction and combining ULK1 inhibition with the senolytic drug ABT-263 leads to apoptosis in cancer cell lines.

MOLECULAR CANCER RESEARCH (2021)

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Article Oncology

Therapeutic Potential of EWSR1-FLI1 Inactivation by CRISPR/Cas9 in Ewing Sarcoma

Saint T. Cervera et al.

Summary: Ewing sarcoma is an aggressive bone cancer affecting children and young adults, characterized by chromosomal translocations producing chimeric oncogenic transcription factors. In this study, genetic inactivation of the EWSR1-FLI1 oncogene using CRISPR/Cas9 technology in Ewing sarcoma cells effectively blocked cell proliferation and induced a senescence phenotype. This suggests that complete inactivation of EWSR1-FLI1 at the cellular level could be a promising therapeutic approach in the future.

CANCERS (2021)

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Review Cell Biology

Applications of CRISPR-Cas9 Technology to Genome Editing in Glioblastoma Multiforme

Nadia Al-Sammarraie et al.

Summary: CRISPR-Cas9 genome editing is crucial in elucidating the genetic regulators of GBM, particularly in vitro systems for identifying novel transcriptional regulators, while in vivo research requires further exploration.

CELLS (2021)

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Article Biochemistry & Molecular Biology

Modulating gene expression in breast cancer via DNA secondary structure and the CRISPR toolbox

Jessica A. Kretzmann et al.

Summary: Breast cancer is the most commonly diagnosed malignancy in women, with the challenge of recurrence and incurability in advanced stages. Transcription factors offer a unique therapeutic opportunity in breast cancer treatment, but there are current limitations to be addressed.

NAR CANCER (2021)

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Article Oncology

Targeted degradation of activating estrogen receptor α ligand-binding domain mutations in human breast cancer

Thomas L. Gonzalez et al.

BREAST CANCER RESEARCH AND TREATMENT (2020)

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Article Oncology

Significance of BRCA2 and RB1 Co-loss in Aggressive Prostate Cancer Progression

Goutam Chakraborty et al.

CLINICAL CANCER RESEARCH (2020)

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Article Biochemistry & Molecular Biology

CRISPR/Cas9-Mediated TERT Disruption in Cancer Cells

Luan Wen et al.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2020)

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Article Genetics & Heredity

ARID1A influences HDAC1/BRD4 activity, intrinsic proliferative capacity and breast cancer treatment response

Sankari Nagarajan et al.

NATURE GENETICS (2020)

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Article Multidisciplinary Sciences

CRISPR-mediated ablation of overexpressed EGFR in combination with sunitinib significantly suppresses renal cell carcinoma proliferation

Bin Liu et al.

PLOS ONE (2020)

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Article Oncology

Global Regulation of the Histone Mark H3K36me2 Underlies Epithelial Plasticity and Metastatic Progression

Salina Yuan et al.

CANCER DISCOVERY (2020)

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Article Oncology

The aryl hydrocarbon receptor promotes inflammation-induced dedifferentiation and systemic metastatic spread of melanoma cells

Miriam Mengoni et al.

INTERNATIONAL JOURNAL OF CANCER (2020)

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Article Oncology

H3.3 G34W Promotes Growth and Impedes Differentiation of Osteoblast-Like Mesenchymal Progenitors in Giant Cell Tumor of Bone

Sima Khazaei et al.

CANCER DISCOVERY (2020)

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Article Oncology

Knockout of EGFL6 by CRISPR/Cas9 Mediated Inhibition of Tumor Angiogenesis in Ovarian Cancer

Wenhui Zhu et al.

FRONTIERS IN ONCOLOGY (2020)

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Review Cell Biology

On the evolution of cellular senescence

Axel Kowald et al.

AGING CELL (2020)

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Article Oncology

Anillin regulates breast cancer cell migration, growth, and metastasis by non-canonical mechanisms involving control of cell stemness and differentiation

Dongdong Wang et al.

BREAST CANCER RESEARCH (2020)

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Article Medicine, Research & Experimental

TGF-β inhibition via CRISPR promotes the long-term efficacy of CAR T cells against solid tumors

Na Tang et al.

JCI INSIGHT (2020)

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