ArticleFrontiers of medicine2023
GDF15 negatively regulates chemosensitivity via TGFBR2-AKT pathway-dependent metabolism in esophageal squamous cell carcinoma.
Article in Frontiers of medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Efficacy of albumin-bound paclitaxel versus paclitaxel in esophageal cancer: a systematic review and meta-analysis.Frontiers in oncology · 2025Pooled it
- Matrix stiffness-induced YEATS2 drives HCC progression via epigenetic activation of the TGFBR2-TAZ-AKT pathway.Cell death and differentiation · 2026Article
- GDF15: A Hijacked Metabo-Hormone Orchestrating Cachexia and Immunosuppression in Cancer.Biomolecules · 2026Review
- Unraveling potent therapeutic potentials of tanshinones, lipophilic abietane diterpenes: a holistic literature review.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- A palmitoylation signature for prognosis immune infiltration and drug sensitivity in esophageal carcinoma.iScience · 2026Article
- Targeting the CAF-GDF15 axis attenuates AKT-mediated mitochondrial rewiring and chemoradiation resistance in esophageal adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2026Article
- Osteocyte-Derived GDF15 Promotes Paclitaxel Resistance, Tumor Growth, and Bone Microenvironment Regulation in Prostate Cancer.Current issues in molecular biology · 2026Article
- The Spleen Promotes Liver Sinusoidal Endothelial Cell Angiogenesis by Stimulating the TGFβ/Smad2/3 Pathway Through GDF15.Journal of gastroenterology and hepatology · 2026Article
- Morusin targeting GDF15 enhances ferroptosis and overcomes cisplatin resistance in NSCLC.Frontiers in pharmacology · 2026Article
- Cigarette smoke extract promotes metastasis and oxaliplatin resistance in colon adenocarcinoma through GDF15/ERBB2/AKT pathway.European journal of medical research · 2025Article
- Ectopic expression of GDF15 in cancer-associated fibroblasts enhances melanoma immunosuppression via the GFRAL/RET cascade.Journal for immunotherapy of cancer · 2025Article
- STC2+ Malignant Cell State Associated with EMT, Tumor Microenvironment Remodeling, and Poor Prognosis Revealed by Single-Cell and Spatial Transcriptomics in Colorectal Cancer.Oncology research · 2025Article
- Uncovering key genes and molecular mechanisms of dendritic cell dysfunction in Esophageal Cancer: implications for Novel Diagnostic and therapeutic strategies.Discover oncology · 2024Article
- A systemic effect for liver senescence.Nature cell biology · 2024Article
- GDF15 induces chemoresistance to oxaliplatin by forming a reciprocal feedback loop with Nrf2 to maintain redox homeostasis in colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Improving the prognosis of pancreatic cancer: insights from epidemiology, genomic alterations, and therapeutic challenges.Frontiers of medicine · 2023Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Treating patients with esophageal squamous cell carcinoma (ESCC) is challenging due to the high chemoresistance. Growth differentiation factor 15 (GDF15) is crucial in the development of various types of tumors and negatively related to the prognosis of ESCC patients according to our previous research. In this study, the link between GDF15 and chemotherapy resistance in ESCC was further explored. The relationship between GDF15 and the chemotherapy response was investigated through in vitro and in vivo studies. ESCC patients with high levels of GDF15 expression showed an inferior chemotherapeutic response. GDF15 improved the tolerance of ESCC cell lines to low-dose cisplatin by regulating AKT phosphorylation via TGFBR2. Through an in vivo study, we further validated that the anti-GDF15 antibody improved the tumor inhibition effect of cisplatin. Metabolomics showed that GDF15 could alter cellular metabolism and enhance the expression of UGT1A. AKT and TGFBR2 inhibition resulted in the reversal of the GDF15-induced expression of UGT1A, indicating that TGFBR2-AKT pathway-dependent metabolic pathways were involved in the resistance of ESCC cells to cisplatin. The present investigation suggests that a high level of GDF15 expression leads to ESCC chemoresistance and that GDF15 can be targeted during chemotherapy, resulting in beneficial therapeutic outcomes.
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