4.8 Article

The RNA-binding protein LRPPRC promotes resistance to CDK4/6 inhibition in lung cancer

Related references

Note: Only part of the references are listed.
Article Biochemistry & Molecular Biology

CDK4/6 inhibitors induce replication stress to cause long-term cell cycle withdrawal

Lisa Crozier et al.

Summary: CDK4/6 inhibitors can induce a prolonged G1 arrest, downregulate replisome components, impair origin licencing, and lead to long-lasting effects on tumor growth. This unexpected ability to induce DNA damage provides a rationale for predicting responsive tumor types and effective combination therapies.

EMBO JOURNAL (2022)

Review Multidisciplinary Sciences

CDK4 and CDK6 kinases: From basic science to cancer therapy

Anne Fassl et al.

Summary: Cyclin-dependent kinases 4 and 6, along with their activation partners, D-type cyclins, play a crucial role in connecting the extracellular environment with the cell cycle machinery. Inhibiting CDK4/6 has shown success in treating hormone receptor-positive breast cancers and may have potential applications in other tumor types. Recent research has shown that CDK4/6 inhibition affects various cellular functions, including tumor cell metabolism and anti-tumor immunity.

SCIENCE (2022)

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)

Article Biochemistry & Molecular Biology

Targeting the miR-34a/LRPPRC/MDR1 axis collapse the chemoresistance in P53 inactive colorectal cancer

Yang Yang et al.

Summary: This study reports a novel mechanism and target related to P53-induced drug resistance and provides corresponding interventional strategies for the precision treatment of colorectal cancer (CRC).

CELL DEATH AND DIFFERENTIATION (2022)

Article Oncology

In vivo efficacy assessment of the CDK4/6 inhibitor palbociclib and the PLK1 inhibitor volasertib in human chordoma xenografts

Thibault Passeri et al.

Summary: This study evaluated the tumor efficacy of the CDK4/6 inhibitor palbociclib and the PLK1 inhibitor volasertib in chordoma patient-derived xenograft (PDX) models. The results showed a significant tumor response to palbociclib in chordoma models with a deletion of CDKN2A/2B genes. However, no tumor response was observed with volasertib in all tested models. Further studies are needed to confirm the efficacy of CDK4/6 inhibitors and understand the resistance mechanisms to palbociclib.

FRONTIERS IN ONCOLOGY (2022)

Article Cell Biology

LncRNA SNHG17 interacts with LRPPRC to stabilize c-Myc protein and promote G1/S transition and cell proliferation

Jin-Yu Liu et al.

Summary: The study reveals that SNHG17 interacts with LRPPRC to enhance c-Myc expression, accelerate G1/S transition and cell proliferation, promoting tumor growth. High levels of SNHG17 or LRPPRC are associated with lower survival rates in HCC patients.

CELL DEATH & DISEASE (2021)

Article Biochemistry & Molecular Biology

LRPPRC regulates redox homeostasis via the circANKHD1/FOXM1 axis to enhance bladder urothelial carcinoma tumorigenesis

Wen-Su Wei et al.

Summary: LRPPRC plays critical roles in regulating UCB redox homeostasis and tumorigenesis by modulating ROS balance, mt-mRNA metabolism, and the circANKHD1/FOXM1 axis to protect UCB cells from oxidative stress. Additionally, LRPPRC is a prognostic factor for UCB and may be a therapeutic target in UCB.

REDOX BIOLOGY (2021)

Article Oncology

Distinct CDK6 complexes determine tumor cell response to CDK4/6 inhibitors and degraders

Xuewei Wu et al.

Summary: Research shows that CDK4/6 inhibitors are particularly effective in tumors with low CDK6 expression, while tumors expressing both CDK4 and CDK6 rely more on CDK6. The study reveals that CDK4/6is and CDK4/6 degraders selectively inhibit CDK6 in tumors where it is highly thermo-unstable and associated with the HSP90-CDC37 complex, but are ineffective in tumor cells expressing thermostable CDK6.

NATURE CANCER (2021)

Article Oncology

In vivo and in vitro inhibition of osteosarcoma growth by the pan Bcl-2 inhibitor AT-101

Laura Masuelli et al.

INVESTIGATIONAL NEW DRUGS (2020)

Review Oncology

Mechanisms of Sensitivity and Resistance to CDK4/6 Inhibition

Monica Alvarez-Fernandez et al.

CANCER CELL (2020)

Article Oncology

Metabolic Adaptations to MEK and CDK4/6 Cotargeting in Uveal Melanoma

Jessica L. F. Teh et al.

MOLECULAR CANCER THERAPEUTICS (2020)

Article Multidisciplinary Sciences

Macrophage secretion of miR-106b-5p causes renin-dependent hypertension

J. Oh et al.

NATURE COMMUNICATIONS (2020)

Article Multidisciplinary Sciences

Aberrant FGFR signaling mediates resistance to CDK4/6 inhibitors in ER plus breast cancer

Luigi Formisano et al.

NATURE COMMUNICATIONS (2019)

Article Cell Biology

MDM2 antagonists overcome intrinsic resistance to CDK4/6 inhibition by inducing p21

Anna E. Vilgelm et al.

SCIENCE TRANSLATIONAL MEDICINE (2019)

Article Chemistry, Multidisciplinary

Proteasome-Independent Protein Knockdown by Small-Molecule Inhibitor for the Undruggable Lung Adenocarcinoma

Wei Zhou et al.

JOURNAL OF THE AMERICAN CHEMICAL SOCIETY (2019)

Article Medicine, Research & Experimental

Mitochondrial Damage Mediated by miR-1 Overexpression in Cancer Stem Cells

Song Zhang et al.

MOLECULAR THERAPY-NUCLEIC ACIDS (2019)

Article Biochemistry & Molecular Biology

TGIF2 promotes the progression of lung adenocarcinoma by bridging EGFR/RAS/ERK signaling to cancer cell stemness

Renle Du et al.

SIGNAL TRANSDUCTION AND TARGETED THERAPY (2019)

Article Chemistry, Multidisciplinary

RNA Chemical Proteomics Reveals the N6-Methyladenosine (m6A)-Regulated Protein-RNA Interactome

A. Emilia Arguello et al.

JOURNAL OF THE AMERICAN CHEMICAL SOCIETY (2017)

Article Multidisciplinary Sciences

CDK4/6 inhibition triggers anti-tumour immunity

Shom Goel et al.

NATURE (2017)

Article Multidisciplinary Sciences

The metabolic function of cyclin D3-CDK6 kinase in cancer cell survival

Haizhen Wang et al.

NATURE (2017)

Article Multidisciplinary Sciences

LRPPRC-mediated folding of the mitochondrial transcriptome

Stefan J. Siira et al.

NATURE COMMUNICATIONS (2017)

Article Cell Biology

Differential Regulation of G1 CDK Complexes by the Hsp90-Cdc37 Chaperone System

Stephen T. Hallett et al.

CELL REPORTS (2017)

Review Oncology

Targeting CDK4 and CDK6: From Discovery to Therapy

Charles J. Sherr et al.

CANCER DISCOVERY (2016)

Review Oncology

Treating cancer with selective CDK4/6 inhibitors

Ben O'Leary et al.

NATURE REVIEWS CLINICAL ONCOLOGY (2016)

Article Medicine, General & Internal

Palbociclib and Letrozole in Advanced Breast Cancer

Richard S. Finn et al.

NEW ENGLAND JOURNAL OF MEDICINE (2016)

Review Biochemistry & Molecular Biology

Targeting the RB-E2F pathway in breast cancer

J. Johnson et al.

ONCOGENE (2016)

Article Medicine, Research & Experimental

Nutrient sensing by the mitochondrial transcription machinery dictates oxidative phosphorylation

Lijun Liu et al.

JOURNAL OF CLINICAL INVESTIGATION (2014)

Editorial Material Oncology

The Kinase-Independent, Second Life of CDK6 in Transcription

Tobias Otto et al.

CANCER CELL (2013)

Article Biochemistry & Molecular Biology

LRPPRC is necessary for polyadenylation and coordination of translation of mitochondrial mRNAs

Benedetta Ruzzenente et al.

EMBO JOURNAL (2012)

Article Multidisciplinary Sciences

Highly tumorigenic lung cancer CD133+ cells display stem-like features and are spared by cisplatin treatment

Giulia Bertolini et al.

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2009)