FAT1 inhibits AML autophagy and proliferation via downregulating ATG4B expression

Review Cell Biology

HIVEP3 as a potential prognostic factor promotes the development of acute myeloid leukemia

Yanfei Tang et al.

Summary: This study revealed that HIVEP3 plays a crucial role in the progression of AML by regulating the TGF-beta/Smad signaling pathway and has prognostic value for AML.

GROWTH FACTORS (2023)

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Article Oncology

Clinical significance of FAT1 gene mutation and mRNA expression in patients with head and neck squamous cell carcinoma

Su Il Kim et al.

Summary: The FAT1 gene has both tumor suppressor and promoter functions in head and neck squamous cell carcinoma (HNSCC). Research has shown that the FAT1 gene signature is associated with prognosis, response to radiotherapy, advanced stage, and human papilloma virus (HPV) status in HNSCC patients.

MOLECULAR ONCOLOGY (2022)

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Article Cell Biology

Targeting autophagy peptidase ATG4B with a novel natural product inhibitor Azalomycin F4a for advanced gastric cancer

Lin Zhong et al.

Summary: This study found that autophagy-related gene 4B (ATG4B) was overexpressed in advanced gastric cancer (GCa) tumors and was associated with poor prognosis. Researchers identified Azalomycin F4a (Am-F4a) as a potent ATG4B inhibitor through screening a natural compound library. Am-F4a effectively inhibited GCa cell autophagy by directly binding to and inhibiting ATG4B, leading to suppressed tumor growth and reduced cell migration and invasion. Additionally, Am-F4a sensitized tumors to chemotherapy.

CELL DEATH & DISEASE (2022)

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Review Oncology

Autophagy in acute myeloid leukemia: a paradoxical role in chemoresistance

Aafreen Khan et al.

Summary: Autophagy is a degradation pathway that is constantly active in cells and plays a crucial role in maintaining cell homeostasis. Its regulation is implicated in various pathological conditions, including cancer, although its role in cancer initiation and development remains controversial. Autophagy acts as a quality control mechanism in the early stages of cancer, but helps cancer cells adapt to stress and survive in later stages, including exposure to anti-cancer drugs.

CLINICAL & TRANSLATIONAL ONCOLOGY (2022)

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Article Gastroenterology & Hepatology

LncRNA FGD5-AS1 enhances the proliferation and stemness of hepatocellular carcinoma cells through targeting miR-223 and regulating the expression of ECT2 and FAT1

Chen-Kun He et al.

Summary: This study explores the mechanism by which long non-coding RNA FGD5-AS1 regulates hepatocellular carcinoma (HCC) cell proliferation and stemness. The results show that FGD5-AS1 is upregulated in HCC and its high expression predicts poor prognosis. Knockdown of FGD5-AS1 inhibits tumor growth and stemness in mice. FGD5-AS1 directly interacts with miR-223 to promote the expression of ECT2 and FAT1 in HCC, enhancing cell proliferation and stemness. This study identifies potential prognostic biomarkers and therapeutic targets for HCC.

HEPATOLOGY RESEARCH (2022)

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Article Cell Biology

FAT1 downregulation enhances sternness and cisplatin resistance in esophageal squamous cell carcinoma

Yuanfang Zhai et al.

Summary: This study found that FAT1 regulates the stemness and drug resistance of esophageal squamous cell carcinoma (ESCC) cells through the Wnt/β-catenin signaling pathway, specifically targeting the expression of ABCC3. These findings suggest that FAT1 and ABCC3 may serve as potential targets for overcoming chemoresistance in ESCC.

MOLECULAR AND CELLULAR BIOCHEMISTRY (2022)

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Review Biochemistry & Molecular Biology

Targeting TGF-β signal transduction for fibrosis and cancer therapy

Dandan Peng et al.

Summary: TGF-beta plays essential roles in early embryonic development, organogenesis, immune regulation, tissue repair, and adult homeostasis. Its involvement in fibrosis and cancer is complex and context-dependent, showing both inhibitory and promoting effects. Therapeutics targeting TGF-beta signaling hold promise in treating fibrosis and cancer, although the development is hindered by potential systemic cytotoxicity.

MOLECULAR CANCER (2022)

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Article Immunology

Upregulation of Atypical Cadherin FAT1 Promotes an Immunosuppressive Tumor Microenvironment via TGF-β

Khushboo Irshad et al.

Summary: FAT1 promotes tumor immune suppression by upregulating the expression and secretion of TGF-beta1/2 in tumor cells, leading to the formation of an immunosuppressive microenvironment. FAT1 expression is also positively correlated with the expression of markers associated with MDSCs.

FRONTIERS IN IMMUNOLOGY (2022)

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Article Oncology

FAT1 Upregulates in Oral Squamous Cell Carcinoma and Promotes Cell Proliferation via Cell Cycle and DNA Repair

Ting Lan et al.

Summary: Previous studies have shown that FAT1 plays a role in tumor suppression or tumorigenesis depending on the context in various cancers. However, its functions in oral squamous cell carcinoma (OSCC) are still unclear. This study aimed to investigate the role of FAT1 in OSCC. The results showed that FAT1 was significantly upregulated in OSCC and correlated with a poor prognosis. Functional experiments revealed that FAT1 promoted cell proliferation and migration while inhibiting apoptosis in OSCC cells. RNA sequencing analysis indicated that FAT1 may affect the cell cycle and DNA repair process in OSCC.

FRONTIERS IN ONCOLOGY (2022)

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Article Multidisciplinary Sciences

Fat1 deletion promotes hybrid EMT state, tumour stemness and metastasis

Ievgenia Pastushenko et al.

Summary: This study reveals that mutation of the FAT1 gene promotes tumor initiation, progression, invasiveness, stemness, and metastasis. Loss of function of FAT1 activates a CAMK2-CD44-SRC axis while inactivates EZH2, playing important roles in the expression of YAP1 and ZEB1.

NATURE (2021)

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Article Oncology

Mutant NPM1-regulated lncRNA HOTAIRM1 promotes leukemia cell autophagy and proliferation by targeting EGR1 and ULK3

Yipei Jing et al.

Summary: Our study investigated the functional and mechanistic roles of the lncRNA HOTAIRM1 in NPM1-mutated AML. We found that HOTAIRM1 is highly expressed in NPM1-mutated AML and is induced in part by mutant NPM1 through KLF5-dependent transcriptional regulation. Importantly, HOTAIRM1 promotes autophagy and proliferation both in vitro and in vivo, acting as a scaffold for EGR1 degradation in the nucleus and as a sponge for miR-152-3p to increase ULK3 expression in the cytoplasm. Overall, our findings suggest that HOTAIRM1 may be a promising therapeutic target for this distinct leukemia subtype.

JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH (2021)

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Article Environmental Sciences

Fat1 suppresses the tumor-initiating ability of nonsmall cell lung cancer cells by promoting Yes-associated protein 1 nuclear-cytoplasmic translocation

Minjie Li et al.

Summary: Fat1 suppresses the tumor-initiating ability of NSCLC cells by activating Hippo signaling.

ENVIRONMENTAL TOXICOLOGY (2021)

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Article Cell & Tissue Engineering

Autonomous TGFβ signaling induces phenotypic variation in human acute myeloid leukemia

Yasuhiro Shingai et al.

Summary: The heterogeneity of AML cells, including varying ESAM expression levels, can be mutually interconverted and regulated by the activation of the TGF beta signaling pathway. Inhibition of TGF beta signaling not only blocks the phenotypic variation of AML cells, but also hinders their proliferation, making it a potential therapeutic target for AML.

STEM CELLS (2021)

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Article Biochemistry & Molecular Biology

AML poor prognosis factor, TPD52, is associated with the maintenance of haematopoietic stem cells through regulation of cell proliferation

Ji Wan Kang et al.

Summary: The study found that elevated TPD52 expression is associated with poor cytogenetic factors in AML patients, particularly affecting the development of HSCs. The results suggest that TPD52 may serve as a novel therapeutic target for AML patients.

JOURNAL OF CELLULAR BIOCHEMISTRY (2021)

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Correction Oncology