ArticleMolecular biology reports2022
FOXM1 mediates GDF-15 dependent stemness and intrinsic drug resistance in breast cancer.
Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- The Regulatory Network of FOXM1: Orchestrating Cancer Progression and Resistance to Therapy.International journal of molecular sciences · 2026Review
- FOXM1 as a candidate dosage rheostat and state selector in breast cancer: linking multilevel regulation to adaptive plasticity and therapy resistance.Frontiers in oncology · 2026Review
- Inhibition of FOXM1 Leads to Suppression of Cell Proliferation, Migration, and Invasion Through AXL/eEF2 Kinase Signaling and Induces Apoptosis and Ferroptosis in GBM Cells.International journal of molecular sciences · 2025Article
- Direct triangular comparison of tissue and serum growth differentiation factor 15 with host factors in colorectal cancer.American journal of cancer research · 2025Article
- Bioinformatics insights intoFrontiers in cell and developmental biology · 2025Article
- Targeting drug resistance in breast cancer: the potential of miRNA and nanotechnology-driven delivery systems.Nanoscale advances · 2024Review
- 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
- FOXM1 mediates methotrexate resistance in osteosarcoma cells by promoting autophagy.Acta biochimica et biophysica Sinica · 2024Article
- GALNT14 in association with GDF-15 promotes stemness and drug resistance through β-catenin signalling pathway in breast cancer.Molecular biology reports · 2024Article
- OTUD7B knockdown inhibits the proliferation and stemness of breast cancer cells by destabilizing FOXM1.Oncology letters · 2024Article
- Role of ABCC5 in cancer drug resistance and its potential as a therapeutic target.Frontiers in cell and developmental biology · 2024Review
- KLF4 suppresses the proliferation of perihilar cholangiocarcinoma by negatively regulating GDF15 and phosphorylating AKT.Oncology reports · 2023Article
- Dysregulated Signalling Pathways Driving Anticancer Drug Resistance.International journal of molecular sciences · 2023Review
- FOXM1: A small fox that makes more tracks for cancer progression and metastasis.Seminars in cancer biology · 2023Review
- Analyzing the Association of Visceral Adipose Tissue Growth Differentiation Factor-15 and MicroRNA in Type 2 Diabetes Mellitus.Journal of obesity & metabolic syndrome · 2023Article
- Visceral Adipose Tissue Molecular Networks and Regulatory microRNA in Pediatric Obesity: An In Silico Approach.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundStemness, a key component of breast cancer (BC) heterogeneity, is responsible for chemoresistance. Growth differentiation factor-15 (GDF-15) induces drug resistance and stemness in BC cells. In this study, the expressions and interactions of GDF-15, FOXM1, and stemness (OCT4 and SOX2), and drug resistance (ABCC5) markers were evaluated in BC. METHODS AND
results40 diagnosed BC patients and 40 healthy controls were included in this study. Serum GDF-15 was significantly raised (p < 0.001) in BC patients. Expressions of GDF-15, OCT4, SOX2, and FOXM1 in BC tissue and cell lines (MCF-7 and MDA-MB-231) were determined by RT-PCR, while phosphorylated AKT (p-AKT) was analyzed by Western blot. Not only were the fold change expressions higher in cancer tissue as compared to surrounding control tissue, but a higher expression was observed for all the genes along with p-AKT in MDA-MB-231 cells compared to MCF-7. Tissue GDF-15 was significantly associated with ABCC5 (p < 0.001), OCT4 (p = 0.002), SOX2 (p < 0.001), and FOXM1 (p < 0.001). To further analyze the signaling pathway involved in stemness and drug resistance in BC, GDF-15 knockdown was performed, which reduced the expression of p-AKT, FOXM1, OCT4 and SOX2, and ABCC5, whereas recombinant GDF-15 treatment reversed the same. In silico analyses in UALCAN revealed a similar picture for these genes to that of BC tissue expression.
conclusionsGDF-15 promotes stemness and intrinsic drug resistance in BC, possibly mediated by the p-AKT/FOXM1 axis.
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Registered trials
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 OpenQuestion graph.