ArticleCell stress & chaperones2023
ORP5 promotes migration and invasion of cervical cancer cells by inhibiting endoplasmic reticulum stress.
Article in Cell stress & chaperones, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Dynamic Shifts in ER-Plasma Membrane Junctions Signaling Define Pro-Metastatic N-Glycosylation and Predict Prostate Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Role of Oxysterol-Binding Protein Family in Cholesterol Metabolism and Cancer Progression: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- ORP5 promotes cardiac hypertrophy by regulating the activation of mTORC1 on lysosome.Journal of advanced research · 2025Article
- Combined spatially resolved metabolomics and spatial transcriptomics reveal the mechanism of RACK1-mediated fatty acid synthesis.Molecular oncology · 2025Article
- Integrated bioinformatics combined with machine learning to analyze shared biomarkers and pathways in psoriasis and cervical squamous cell carcinoma.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ORP5 is a transmembrane protein anchored to the endoplasmic reticulum, which mainly functions as a lipid transporter and has reportedly been linked to cancer. However, the specific mechanism of ORP5 action in cervical cancer (CC) is unclear. In this study, we found that ORP5 promotes the migration and invasive ability of CC cells in vitro and in vivo. In addition, ORP5 expression was linked to endoplasmic reticulum stress, and ORP5 encouraged CC metastasis by inhibiting endoplasmic reticulum stress. Mechanistically, ORP5 inhibited endoplasmic reticulum stress in CC cells by stimulating ubiquitination and proteasomal degradation of SREBP1 to reduce its expression. In conclusion, ORP5 promotes the malignant progression of CC by inhibiting endoplasmic reticulum stress, providing a therapeutic target and strategy for CC treatment.
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Registered trials
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