ArticleDiscover oncology2024
RPN1 promotes the proliferation and invasion of breast cancer cells by activating the PI3K/AKT/mTOR signaling pathway.
Article in Discover oncology, 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, 10 citations in OpenAlex.
- Disulfidptosis: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Comprehensive analysis of disulfidptosis-related genes identifies clinically actionable prognostic biomarkers in cholangiocarcinoma.Discover oncology · 2026Article
- Transcriptomic profiles of endocrine-resistant breast cancer.BMC cancer · 2025Article
- Disulfidptosis-related genes RPN1 inhibits the progression of hepatocellular carcinoma by regulating cell cycle, may be a new therapeutic targets.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- KLF4 promotes cisplatin resistance by activating mTORC1 signaling in ovarian cancer.Discover oncology · 2024Article
- Prognostic and therapeutic model based on disulfidptosis-related genes for patients with clear cell renal cell carcinoma.Heliyon · 2024Article
- Article
- Dissecting the functions and regulatory mechanisms of disulfidoptosis-related RPN1 in pan-cancer: modulation of immune microenvironment and cellular senescence.Frontiers in immunology · 2024Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ribophorin I (RPN1), a part of an N-oligosaccharyl-transferase complex, plays a vital role in the development of multiple cancers. However, its biological role in breast cancer has not been completely clarified. The RPN1 expression level was measured in breast cancer tissues and breast cancer cell lines (MCF7) using RT-qPCR. After down-regulating RPN1 expression by shRNA, the effects of RPN1 on the proliferation, migration and invasion of MCF7 cells were examined. Mechanistically, we assessed the effect of RPN1 on the PI3K/ AKT/mTOR signaling pathway. We found that RPN1 level was up-regulated in breast cancer tissues and cells compared with adjacent non-tumor tissues or MCF10A cells. RPN1 knockdown induced apoptosis and attenuated the proliferation, migration, and invasion of MCF7 cells. Moreover, RPN1 knockdown lowered the levels of p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR, which were rescued by 740Y-P, a PI3K activator. 740Y-P also reversed the effects of RPN1 knockdown on apoptosis, proliferation, migration, and invasion in MCF7 cells. Taken together, RPN1 promotes the proliferation, migration, and invasion of breast cancer cells via the PI3K/AKT/mTOR signaling pathway.
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