ArticleCancer science2025
Transferrin Receptor Promotes Endometrial Cancer Proliferation by Activating the Iron-Dependent PI3K/AKT/mTOR Signaling Pathway.
Article in Cancer science, 2025. 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.
- Transferrin receptor 1: an emerging therapeutic target in cancer beyond iron metabolism.Cancer cell international · 2026Review
- TFRC promotes ferroptosis to suppress breast cancer bone metastasis via the activation of HIF-1 pathway.Breast cancer research : BCR · 2026Article
- Dysregulation of ferroptosis-related genes and the ACSL4-mediated ferroptosis-PD-L1 axis in prostate cancer pathogenesis.Cancer cell international · 2026Article
- Ferroptosis in Human Diseases: Fundamental Roles and Emerging Therapeutic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Molecular mechanisms by which C1orf112 promotes endometrial cancer progression and the development and validation of a clinical scoring model.Clinical epigenetics · 2025Article
- Identification and validation of ubiquitination-related genes for predicting cervical cancer outcome.Frontiers in genetics · 2025Article
- Decoding the Anti-Tumour Mechanism of ɑ-Solanine: SRC Inhibition and Ferroptosis Induction in Colon Cancer.IET systems biologyArticle
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Aberrant iron metabolism is frequently observed in cancers, including endometrial cancer (EC). However, the role of transferrin receptor (TFRC), a key regulator of iron metabolism, remains unclear in endometrial cancer. We found transferrin receptor expression was significantly upregulated in endometrial cancer tissues compared to adjacent nontumor tissues, and high transferrin receptor levels were associated with poor prognosis. Functional studies revealed that transferrin receptor knockdown impaired endometrial cancer cell proliferation in vitro and in vivo, while transferrin receptor overexpression enhanced endometrial cancer cell proliferation. Mechanistically, transferrin receptor activated the PI3K/AKT/mTOR signaling pathway, as its knockdown suppressed the pathway, and rapamycin, an mTOR inhibitor, reversed transferrin receptor-induced pathway activation and proliferation. Modulation of the labile iron pool by ferric ammonium citrate (FAC) or deferoxamine (DFO) rescued transferrin receptor-induced biological effects. Additionally, AURKA was identified as a regulator of transferrin receptor expression. These findings demonstrate the oncogenic role of transferrin receptor in endometrial cancer and suggest that targeting iron homeostasis and the PI3K/AKT/mTOR pathway may represent potential therapeutic strategies for endometrial cancer.
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