ArticleCell death & disease2018
SIRT1 suppresses the migration and invasion of gastric cancer by regulating ARHGAP5 expression.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 67 citations in OpenAlex.
- Targeted inhibition of MDSC-derived exosomal miR-155-5p restrains epithelial-mesenchymal transition in hormone receptor-positive breast cancer by regulating SIRT1.Materials today. Bio · 2025Article
- SLC6A19-mediated tryptophan uptake suppresses renal cell carcinoma metastasis via activating NADOncogenesis · 2025Article
- The crosstalk between MicroRNAs and sirtuins: a bit unexpected therapeutic target for cardiovascular diseases.European journal of medical research · 2025Review
- Delactylase effects of SIRT1 on a positive feedback loop involving the H19-glycolysis-histone lactylation in gastric cancer.Oncogene · 2025Article
- Suppression of FOXO1 activity by SIRT1-mediated deacetylation weakening the intratumoral androgen autocrine function in glioblastoma.Cancer gene therapy · 2025Article
- The role of SIRT1 in the development of gastrointestinal tumors.Frontiers in cell and developmental biology · 2025Review
- Liposomal Nanoparticle Delivery of Ginkgo Flavone Glycosides Enhances SIRT1 Activation and Improves Diabetic Cardiomyopathy.International journal of nanomedicine · 2025Article
- Exploring COX-Independent Pathways: A Novel Approach for Meloxicam and Other NSAIDs in Cancer and Cardiovascular Disease Treatment.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Integrated analysis identified the role of three family members of ARHGAP in pancreatic adenocarcinoma.Scientific reports · 2024Article
- MicroRNA-34 and gastrointestinal cancers: a player with big functions.Cancer cell international · 2024Review
- Intergenomic signatures of coevolution between Tasmanian devils and an infectious cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- The dual role of sirtuins in cancer: biological functions and implications.Frontiers in oncology · 2024Review
- A strategy for the treatment of gastrointestinal cancer: Targeting tumor senescent cells.Frontiers in molecular biosciences · 2023Review
- Transcription factor c-Jun modulates GLUT1 in glycolysis and breast cancer metastasis.BMC cancer · 2022Article
- Sirtuins (SIRTs) As a Novel Target in Gastric Cancer.International journal of molecular sciences · 2022Review
- Review
- The prognostic implications of SIRTs expression in breast cancer: a systematic review and meta-analysis.Discover oncology · 2022Article
- TGFBR1*6A as a modifier of breast cancer risk and progression: advances and future prospects.NPJ breast cancer · 2022Review
- miR-135b-5p Targets SIRT1 to Inhibit Deacetylation of c-JUN and Increase MMP7 Expression to Promote Migration and Invasion of Nasopharyngeal Carcinoma Cells.Molecular biotechnology · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) ranks among the top five malignant tumors worldwide by the incidence and mortality rate. However, the mechanisms underlying its progression are poorly understood. In this study, we investigated the role of SIRT1, a class III deacetylase, in the invasion and metastasis of GC. Here, we found that knockdown of SIRT1 promoted GC cell migration and invasion in vitro and metastasis in vivo. Forced expression of SIRT1 in GC cells had the opposite effects. Then, we used mRNA microarray to identify the target genes that are regulated by SIRT1 and found that ARHGAP5 was downregulated by SIRT1. The results of the mRNA microarray were confirmed in several GC cell lines. Furthermore, SIRT1 inhibited the expression of ARHGAP5 by physically associating with transcription factor c-JUN and deacetylating and inhibiting the transcriptional activity of c-JUN. Then the expression dynamics and clinical significance of ARHGAP5 were analyzed using clinical samples and database. The expression of ARHGAP5 was increased in GC, and positively correlated with tumor size, tumor infiltration, lymph node metastasis, and clinical stage. And multivariate analyses indicated that ARHGAP5 served as an independent prognostic marker of GC. In addition, the biological effects of ARHGAP5 in SIRT1-mediated inhibition of GC migration and invasion were investigated using both in vitro and in vivo models. Silencing of ARHGAP5 considerably inhibited the migration and invasion of GC, and ARHGAP5 was found to be involved in the SIRT1-mediated inhibition of GC migration and invasion. Our results indicate that SIRT1 suppresses migration and invasion of GC by downregulating ARHGAP5 through an interaction with c-JUN, and these phenomena represent a novel mechanism of the antitumor action of SIRT1.
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