ArticleCell death & disease2025
TFE3 and HIF1α regulates the expression of SHMT2 isoforms via alternative promoter utilization in ovarian cancer cells.
Article in Cell death & disease, 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.
- Bidirectional Feedback Between Metabolic Reprogramming and Epithelial-Mesenchymal Transition: From Mechanisms to Therapeutic Interventions.Molecules (Basel, Switzerland) · 2026Review
- Serine Hydroxymethyltransferase (SHMT) in biology and disease: molecular mechanisms and therapeutic targeting.Journal of translational medicine · 2026Review
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- Advancing the frontiers of ovarian cancer therapy: a comprehensive synthesis of emerging cell death paradigms.Oncology reviews · 2026Review
- Multifaceted role of serine hydroxymethyltransferase in health and disease.Molecules and cells · 2025Review
- RNA-mediated inhibition of mitochondrial SHMT2 impairs cancer cell proliferation.Cell death discovery · 2025Article
- Comparative RNA-Seq Analysis of Colon Spheroids and Patient-derived Tissues Identifies Non-Canonical Transcript Isoforms of Protein-Coding Genes Implicated in Colon Carcinogenesis.Cancer informatics · 2025Article
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8 authors.
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Abstract
Ovarian cancer ranks first lethally among gynecological malignancies. Platinum-based chemotherapy constitutes the first-line therapeutic regime. However, primary or acquired resistance seriously affects the survival rate of patients with ovarian cancer. Serine hydroxy methyltransferase (SHMT) catalyzes conversion of serine to glycine and is responsible for production of S-adenosylmethionine (SAM) for methylation. There are cytosolic SHMT1 and mitochondrial SHMT2 in human. Alternative promoter usage is a proteome-expanding mechanism that allows multiple pre-mRNAs to be transcribed from a single gene. The current study demonstrated that cisplatin-sensitive and cisplatin-resistant ovarian cancer cells expressed discrete SHMT2 isoforms, which was ascribed to the selective utilization of SHMT2 alternative promoters. SHMT2 isoforms exerted somewhat paradoxical roles in ovarian cancer cells, with tumor-suppressive role of isoform 1, and tumor-promotive role of isoform 3. In addition, the current study demonstrated that SHMT2 alternative promoter usage mediated by HIF1α and TFE3 might represent adaptive response of ovarian cancer cells to metabolic stress. Collectively, regulation of SHMT2 isoform expression via alternative promoter usage by transcription factors HIF1α and TFE3 provides a novel basis and potential drug targets for the clinical treatment of platin-resistant ovarian cancer.
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