ArticleBioengineered2021
Fat mass and obesity-associated protein (FTO) mediates signal transducer and activator of transcription 3 (STAT3)-drived resistance of breast cancer to doxorubicin.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 43 citations in OpenAlex.
- Fat Mass and Obesity-Associated Protein Contributes to Tumorigenesis and Drug Resistance of Diffuse Large B-Cell Lymphoma by Suppressing N6-Methyladenosine Methylation of Myc.The Kaohsiung journal of medical sciences · 2026Article
- Methylation marks breast cancer metastasis: The roles of mThe Journal of biological chemistry · 2026Review
- Targeting epigenetic methylation: emerging diagnosis and therapeutic strategies in cancer.Experimental hematology & oncology · 2026Review
- Reader-dependent functional duality of FTO: a context-switching node at the intersection of immune evasion and therapeutic resistance.Frontiers in immunology · 2026Review
- FTO promotes the progression of triple-negative breast cancer by regulating the m6A methylation of NFKBIE.Clinical and experimental medicine · 2025Article
- JAK2 Inhibition Augments the Anti-Proliferation Effects by AKT and MEK Inhibition in Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2025Article
- RNA epigenetic modifications as dynamic biomarkers in cancer: from mechanisms to clinical translation.Biomarker research · 2025Review
- Dynamic multilayered control of mProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Advances in the Understanding of the Pathogenesis of Triple-Negative Breast Cancer.Cancer medicine · 2024Review
- Decoding the epitranscriptome: a new frontier for cancer therapy and drug resistance.Cell communication and signaling : CCS · 2024Review
- Enhanced anti-tumor efficacy of S3I-201 in breast cancer mouse model through Wharton jelly- exosome.Cancer cell international · 2024Article
- Functions and mechanisms of RNA mInternational journal of oncology · 2024Review
- Insights into the mCell & bioscience · 2024Review
- GAS5 regulated by FTO-mediated m6A modification suppresses cell proliferation via the IGF2BP2/QKI axis in breast cancer.Discover oncology · 2024Article
- Small molecule inhibitors targeting mJournal of hematology & oncology · 2024Review
- Targeting RNA modifications with pharmacological agents: New frontiers in cancer therapy.Cancer medicine · 2024Review
- Lactylation-driven FTO targets CDK2 to aggravate microvascular anomalies in diabetic retinopathy.EMBO molecular medicine · 2024Article
- Potential therapeutic targets of the JAK2/STAT3 signaling pathway in triple-negative breast cancer.Frontiers in oncology · 2024Review
- FTO diversely influences sensitivity of neuroblastoma cells to various chemotherapeutic drugs.Frontiers in pharmacology · 2024Article
- m6A eraser FTO impairs gemcitabine resistance in pancreatic cancer through influencing NEDD4 mRNA stability by regulating the PTEN/PI3K/AKT pathway.Journal of experimental & clinical cancer research : CR · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive activation of signal transducer and activator of transcription 3 (STAT3) is implicated in breast cancer (BC) chemoresistance, but its underlying mechanism is not fully understood. There are STAT3 binding sites in fat mass and obesity-associated protein (FTO) promoter region, thus STAT3 may regulate the transcription of FTO. This study aimed to investigate the correlation between FTO and STAT3 in BC chemoresistance. Herein, FTO and STAT3 were highly expressed in doxorubicin-resistant BC (BC-DoxR) cells. CHIP assay verified the binding between STAT3 and FTO promoter in BC-DoxR cells. Dual luciferase reporter assay showed that FTO promoter activity was inhibited by S3I-201 (STAT3 inhibitor) but enhanced by epidermal growth factor (EGF, STAT3 activator) in BC-DoxR and BC cells. FTO mRNA and protein expression were suppressed by S3I-201 in BC-DoxR cells and EGF-stimulated BC cells. Notably, FTO regulated total N6-methyladenosine (m6A) levels in BC-DoxR and BC cells but could not affect STAT3 mRNA expression, indicating that FTO was not involved in the m6A modification of STAT3. However, FTO could activate STAT3 signaling in BC-DoxR and BC cells. Besides, FTO knockdown inhibited the doxorubicin resistance of BC-DoxR cells, while FTO overexpression enhanced the doxorubicin resistance and weakened the doxorubicin sensitivity of BC cells. Moreover, decreased doxorubicin resistance by STAT3 knockdown was abolished by FTO overexpression and decreased doxorubicin sensitivity by STAT3 overexpression was reversed by FTO knockdown, indicating that FTO was implicated in STAT3-mediated doxorubicin resistance and impairment of doxorubicin sensitivity of BC cells. Altogether, our findings provide a mechanism underlying BC doxorubicin resistance.
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