ArticleJournal of experimental & clinical cancer research : CR2018
RIF1 promotes human epithelial ovarian cancer growth and progression via activating human telomerase reverse transcriptase expression.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- The Bidirectional Role of Cellular Senescence in the Treatment of Ovarian Cancer.Biomedicines · 2026Review
- Deciphering the Pleiotropic Role ofCells · 2026Article
- Dysregulated Alternative Splicing in Breast Cancer Subtypes of RIF1 and Other Transcripts.International journal of molecular sciences · 2025Article
- Sustained inactivation of the Polycomb PRC1 complex induces DNA repair defects and genomic instability in epigenetic tumors.Histochemistry and cell biology · 2024Article
- Vaginal microbiota and gynecological cancers: a complex and evolving relationship.Infectious agents and cancer · 2024Review
- Sustained inactivation of the Polycomb PRC1 complex induces DNA repair defects and genomic instability in epigenetic tumors.Research square · 2024Article
- Shedding Light on the Interaction Between Rif1 and Telomeres in Ovarian Cancer.Aging and disease · 2024Review
- The emerging roles and potential applications of circular RNAs in ovarian cancer: a comprehensive review.Journal of cancer research and clinical oncology · 2023Review
- The Relevance of Telomerase and Telomere-Associated Proteins in B-Acute Lymphoblastic Leukemia.Genes · 2023Review
- cAMP-Dependent Signaling and Ovarian Cancer.Cells · 2022Review
- SPR Analysis of SUMO-Murine Rap1-Interacting Factor 1 C-Terminal Domain Interaction with G4.Biosensors · 2022Article
- La protein regulates protein expression by binding with the mRNAs of target genes and participates the pathological process of ovarian cancer.Frontiers in oncology · 2022Article
- RIF1 Links Replication Timing with Fork Reactivation and DNA Double-Strand Break Repair.International journal of molecular sciences · 2021Review
- A multi-omics study delineates new molecular features and therapeutic targets for esophageal squamous cell carcinoma.Clinical and translational medicine · 2021Article
- A Study of hTERT Promoter Methylation in Circulating Tumour DNAs of Patients with Ovarian Magnificent Tumour.OncoTargets and therapy · 2020Article
- Vaginal microbiomes and ovarian cancer: a review.American journal of cancer research · 2020Review
- Deiminated proteins in extracellular vesicles and serum of llama (Lama glama)-Novel insights into camelid immunity.Molecular immunology · 2020Article
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6 authors.
Funding
Abstract
backgroundHuman telomerase reverse transcriptase (hTERT) is highly expressed in over 80% of tumors, including human epithelial ovarian cancer (EOC). However, the mechanisms through which hTERT is up-regulated in EOC and promotes tumor progression remain unclear. The aim of this study is to identify RIF1 as a novel molecular target that modulate hTERT signaling and EOC growth.
methodsRIF1 expression in ovarian cancer, benign and normal ovarian tissues was examined by immunohistochemistry. The biological role of RIF1 was revealed by MTS, colony formation and sphere formation assays. Luciferase reporter assay and chromatin immunoprecipitation (CHIP) assay were used to verify RIF1 as a novel hTERT promoter-binding protein in EOC cells. The role of RIF1 on tumorigenesis in vivo was detected by the xenograft model.
resultsRIF1 expression is upregulated in EOC tissues and is closely correlated with FIGO stage and prognosis of EOC patients. Functionally, RIF1 knockdown suppressed the expression and promoter activity of hTERT and consequently inhibited the growth and CSC-like traits of EOC cells. RIF1 knockdown also inhibited tumorigenesis in xenograft model. RIF1 overexpression had the opposite effect. Luciferase reporter assay and ChIP assay verified RIF1 directly bound to hTERT promoter to upregulate its expression. The rescue experiments suggested hTERT overexpression rescued the inhibition of EOC cell growth and CSC-like traits mediated by RIF1 knockdown. Consistently, hTERT knockdown abrogated the RIF1-induced promotion of EOC cell growth and CSC-like traits.
conclusionsRIF1 promotes EOC progression by activating hTERT and the RIF1/hTERT pathway may be a potential therapeutic target for EOC patients.
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