ArticleGenes & genomics2022
Rab11a promotes the malignant progression of ovarian cancer by inducing autophagy.
Article in Genes & genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Where and how do mammalian cells shape autophagosomes?The Journal of biological chemistry · 2026Review
- Advancing the frontiers of ovarian cancer therapy: a comprehensive synthesis of emerging cell death paradigms.Oncology reviews · 2026Review
- Autophagy modulation in gynaecologic oncology: insights into immune regulation and therapeutic potential.Frontiers in immunology · 2026Review
- Urinary exosomal RAB11A serves as a novel non-invasive biomarker for diagnosis, treatment response monitoring, and prognosis in small cell lung cancer.Clinical proteomics · 2025Article
- SSLpheno: a self-supervised learning approach for gene-phenotype association prediction using protein-protein interactions and gene ontology data.Bioinformatics (Oxford, England) · 2023Article
- Role of autophagy and its regulation by noncoding RNAs in ovarian cancer.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Machine-Learning-Based Identification of Key Feature RNA-Signature Linked to Diagnosis of Hepatocellular Carcinoma.Journal of clinical and experimental hepatologyArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRab11a is a novel identified tumorigenic factor involved in different cancers.
objectiveThis study aimed to assess the biological function of Rab11a in ovarian cancer (OC).
methodsGEPIA database and real-time PCR were used to determine Rab11a expression in OC tissues and normal ovarian tissues. CCK-8, cell cycle, wound healing, transwell, and enzyme linked immunosorbent assay were used to detect the effects of Rab11a knockdown or overexpression on the proliferation, migration, and invasion of OC cells. Western blot analysis of autophagy-related markers and immunofluorescence staining of LC3 were performed to determine autophagy induction in Rab11a-silenced or overexpressed OC cells. Moreover, autophagy inhibitor 3-MA was employed to clarify the effects of Rab11a-regulated autophagy on the malignant phenotypes of OC cells.
resultsThe mRNA level of Rab11a was increased in tumor tissues from OC patients as compared to the normal ovarian tissues. Knockdown of Rab11a in OVCAR-3 cells inhibited the growth of OC cells and led to cell cycle arrest, accompanied by reduced expression of PCNA and Cyclin D1. Rab11a deficiency suppressed migration and invasion of OC cells, accompanied by decreased secretion of MMP-2 and MMP-9. Silence of Rab11a impeded autophagy induction, as evidenced by decreased LC3 puncta formation, reduced abundance of LC3II and Beclin1, and increased p62 protein expression. In contrast, the ectopic expression of Rab11a in A2780 cells exerted opposite effects. Interestingly, autophagy inhibitor 3-MA abolished the effects of Rab11a overexpression on autophagy, proliferation, migration, and invasion.
conclusionsRab11a promotes the malignant phenotypes of OC cells by inducing autophagy.
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