ArticleJournal of cellular and molecular medicine2022
RASSF4 inhibits cell proliferation and increases drug sensitivity in colorectal cancer through YAP/Bcl-2 pathway.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
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- RASSF4 Suppresses Gastric Tumor Growth through Activation of Chk2-p53 Signaling Axis.Cancer research and treatment · 2026Article
- BCL-2 and BCL-xL in Cancer: Regulation, Function, and Therapeutic Targeting.International journal of molecular sciences · 2026Review
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- Inhibitory Effect and Mechanism of the Down-Regulation of TRIM32 in Colorectal Cancer.International journal of molecular sciences · 2025Article
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- 4-1BB-encoding CAR causes cell death via sequestration of the ubiquitin-modifying enzyme A20.Cellular & molecular immunology · 2024Article
- Bcl-2 dependent modulation of Hippo pathway in cancer cells.Cell communication and signaling : CCS · 2024Article
- Role of YAP Signaling in Regulation of Programmed Cell Death and Drug Resistance in Cancer.International journal of biological sciences · 2024Review
- Nitric oxide inhibits FTO demethylase activity to regulate NRedox biology · 2023Article
- RASSF4 inhibits cell proliferation and increases drug sensitivity in colorectal cancer through YAP/Bcl-2 pathway.Journal of cellular and molecular medicine · 2022Article
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7 authors at 1 institution in 1 country.
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Abstract
The RASSF family proteins have been implicated in the development of human cancers. To date, the expression pattern and biological significance of RASSF4 in colorectal cancers (CRC) have not been fully investigated. In the current study, we explored expression pattern of RASSF4 in 118 CRC specimens and 30 adjacent 'normal' colon tissues by immunohistochemistry. The results showed that RASSF4 was downregulated in CRC tissues compared with adjacent 'normal' tissues. RASSF4 downregulation significantly associated with advanced tumour-node-metastasis (TNM) stage, T status, positive node status and high Ki-67 index. Analysis of TCGA dataset also supported RASSF4 downregulation in CRC tissues. Ectopically expressed RASSF4 in LoVo cells inhibited cell growth, colony formation, cell cycle progression and increased the sensitivity to 5-FU treatment. Annexin V/PI apoptosis assay showed that RASSF4 overexpression increased 5-FU-induced apoptosis and downregulated the mitochondrial membrane potential. In addition, Western blot demonstrated that RASSF4 overexpression repressed YAP and Bcl-2 while upregulating p21 expression. YAP knockdown abolished the role of RASSF4 on Bcl-2. ChIP assay showed that TEAD4, a major YAP binding transcription factor, could bind to the promoter regions of Bcl-2. In conclusion, our data showed that RASSF4 was downregulated in human CRC. RASSF4 regulated malignant behaviour through YAP/Bcl-2 signalling in CRC cells.
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