ArticleCell death & disease2024
RAB17 promotes endometrial cancer progression by inhibiting TFRC-dependent ferroptosis.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Organoids: Current Applications and Future Directions.MedComm · 2026Review
- Effect of the miR‑26a/b‑5p‑STAT3‑YKL‑40 regulatory axis on proliferation, migration, and invasion of endometrial cancer cells.Oncology reports · 2026Article
- TFRC promotes ferroptosis to suppress breast cancer bone metastasis via the activation of HIF-1 pathway.Breast cancer research : BCR · 2026Article
- Mammalian evolution and human mutation burden in Rab GTPases.Biochemistry and biophysics reports · 2026Article
- Transferrin receptor serves a role in promoting PANoptosis in thyroid cancer.Oncology letters · 2026Article
- USP26-mediated stabilization of RAD51 promotes endometrial cancer progression and limits ferroptosis.Frontiers in oncology · 2026Article
- The prognostic significance of JAML and its role in remodeling the immune microenvironment via the cGAS-STING pathway in endometrial cancer.Frontiers in immunology · 2026Article
- LMO4 promotes OSCC progression by inducing RAB17 degradation and ferroptosis resistance.Cell death & disease · 2025Article
- LOXL1-AS1 suppresses ferroptosis in cervical cancer through m6A-dependent regulation of TFRC.Journal of molecular histology · 2025Article
- The Role of Ferroptosis in Women's Health and Diseases.MedComm · 2025Review
- Prognostic significance and immune infiltration analysis of HMGA2 in endometrial cancer.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Studies have indicated that RAB17 expression levels are associated with tumor malignancy, and RAB17 is more highly expressed in endometrial cancer (EC) tissues than in peritumoral tissues. However, the roles and potential mechanisms of RAB17 in EC remain undefined. The present study confirmed that the expression of RAB17 facilitates EC progression by suppressing cellular ferroptosis-like alterations. Mechanistically, RAB17 attenuated ferroptosis in EC cells by inhibiting transferrin receptor (TFRC) protein expression in a ubiquitin proteasome-dependent manner. Because EC is a blood-deprived tumor with a poor energy supply, the relationship between RAB17 and hypoglycemia was investigated. RAB17 expression was increased in EC cells incubated in low-glucose medium. Moreover, low-glucose medium limited EC cell ferroptosis and promoted EC progression through the RAB17-TFRC axis. The in vitro results were corroborated by in vivo studies and clinical data. Overall, the present study revealed that increased RAB17 promotes the survival of EC cells during glucose deprivation by inhibiting the onset of TFRC-dependent ferroptosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.