ArticleOncoTargets and therapy2019
CHFR promotes the migration of human gastric cancer cells by inducing epithelial-to-mesenchymal transition in a HDAC1-dependent manner.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- CHFR drives gastric cancer stemness and hepatic metastasis by suppressing ITCH-mediated ubiquitination and degradation of OCT4.Biology direct · 2026Article
- CHFR promotes metastasis of human gastric carcinoma by activating AKT and ERK via NRF2- ROS axis.BMC gastroenterology · 2023Article
- UPS: Opportunities and challenges for gastric cancer treatment.Frontiers in oncology · 2023Review
- Association between eight hypermethylation-related genes and gastric cancer: a systematic review and meta-analysis.Translational cancer research · 2022Article
- Regulation of epithelial-mesenchymal transition by protein lysine acetylation.Cell communication and signaling : CCS · 2022Review
- Suppression of histone deacetylase 1 by JSL-1 attenuates the progression and metastasis of cholangiocarcinoma via the TPX2/Snail axis.Cell death & disease · 2022Article
- Roles of E3 ubiquitin ligases in gastric cancer carcinogenesis and their effects on cisplatin resistance.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Development of an Individualized Ubiquitin Prognostic Signature for Clear Cell Renal Cell Carcinoma.Frontiers in cell and developmental biology · 2021Article
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6 authors.
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Abstract
backgroundPrevious studies have illustrated that checkpoint with forkhead-associated and ring finger domains (CHFR) was frequently silenced in several cancer types due to promoter hypermethylation and functions as a tumor suppressor gene. However, the data from the public dataset reveal that CHFR is highly expressed in human gastric cancer specimens, and the biological function of CHFR in gastric cancer is still not well understood. MATERIALS AND
methodsThe clinical association between CHFR expression and the overall survival of gastric cancer patients as well as cancer metastasis was analyzed according to public datasets. The CHFR expression in clinical specimens and human gastric cancer cell lines was detected by immunohistochemistry and Western blotting, respectively. Gain (overexpression) and loss (silencing) of function experiments were used to elucidate the role of CHFR in gastric cancer. The migration ability of gastric cancer cells was determined by wound healing and transwell assays. Cell cycle distribution was analyzed using fluorescence-activated cell sorting experiment. The expression of the proteins in cancer cells was measured using Western blot analysis.
resultsAccording to the analysis from Kaplan-Meier plotter dataset, CHFR expression was negatively associated with overall survival of gastric cancer patients. Our data revealed that exogenous expression of CHFR not only arrested cell cycle but also led to dramatically enhanced cell migration, while silencing of CHFR significantly inhibited cell migration in gastric cancer cells. This result is consistent with the data from the Human Cancer Metastasis Dataset, in which CHFR level is found to significantly increase in metastatic gastric cancer. The overexpression of CHFR promoted epithelial-mesenchymal transition (EMT) in both SGC-7901 and AGS cells, while HDAC1 was inhibited. Interestingly, suberoylanilide hydroxamic acid, a HDAC1 antagonist, could effectively increase cell migration in both cell lines via enhancement of EMT.
conclusionOur data indicated that CHFR exerted positive effects on cell migration of human gastric cancer by promoting EMT via downregulating HDAC1.
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