ArticleCell communication and signaling : CCS2024
SUMOylation of annexin A6 retards cell migration and tumor growth by suppressing RHOU/AKT1-involved EMT in hepatocellular carcinoma.
Article in Cell communication and signaling : CCS, 2024. 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, 12 citations in OpenAlex.
- Article
- Integrated network pharmacology, molecular docking, and experimental validation reveal the antifungal and anti-inflammatory mechanisms of Camellia oleifera seed extracts against oral thrush.Scientific reports · 2026Article
- An Advanced Network Pharmacology Study Reveals the Multi-Pathway and Multi-Gene Regulatory Mechanism of Jinbai Heat-clearing Prescription in HPV-induced Cervical Cancer via Molecular Docking and Microarray Data Analysis.Current medicinal chemistry · 2026Article
- Mechanism of interaction between ANXA6 and cGAS to regulate STING signaling pathway and promote ferroptosis in cervical cancer.Cancer cell international · 2025Article
- SENP1: A perspective from immune cells to disease (Review).Oncology reports · 2025Review
- SENP1-mediated deSUMOylation of YBX1 promotes colorectal cancer development through the SENP1-YBX1-AKT signaling axis.Oncogene · 2025Article
- SENP1 inhibits aerobic glycolysis in AβCell biology and toxicology · 2025Article
- The SUMO Family: Mechanisms and Implications in Thyroid Cancer Pathogenesis and Therapy.Biomedicines · 2024Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe protein annexin A6 (AnxA6) is involved in numerous membrane-related biological processes including cell migration and invasion by interacting with other proteins. The dysfunction of AnxA6, including protein expression abundance change and imbalance of post-translational modification, is tightly related to multiple cancers. Herein we focus on the biological function of AnxA6 SUMOylation in hepatocellular carcinoma (HCC) progression.
methodsThe modification sites of AnxA6 SUMOylation were identified by LC-MS/MS and amino acid site mutation. AnxA6 expression was assessed by immunohistochemistry and immunofluorescence. HCC cells were induced into the epithelial-mesenchymal transition (EMT)-featured cells by 100 ng/mL 12-O-tetradecanoylphorbol-13-acetate exposure. The ability of cell migration was evaluated under AnxA6 overexpression by transwell assay. The SUMO1 modified AnxA6 proteins were enriched from total cellular proteins by immunoprecipitation with anti-SUMO1 antibody, then the SUMOylated AnxA6 was detected by Western blot using anti-AnxA6 antibody. The nude mouse xenograft and orthotopic hepatoma models were established to determine HCC growth and tumorigenicity in vivo. The HCC patient's overall survival versus AnxA6 expression level was evaluated by the Kaplan-Meier method.
resultsLys579 is a major SUMO1 modification site of AnxA6 in HCC cells, and SUMOylation protects AnxA6 from degradation via the ubiquitin-proteasome pathway. Compared to the wild-type AnxA6, its SUMO site mutant AnxA6
conclusionsAnxA6 deSUMOylation contributes to HCC progression and EMT phenotype, and the combination of AnxA6 and SENP1 is a better tumor biomarker for diagnosis of HCC grade malignancy and prognosis.
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