ArticleOncology research2026
Targeting SRC/STAT3 Signaling Impairs Cancer Stem Cell Activity by Downregulation of Hexokinase-2 in Radioresistant Triple-Negative Breast Cancer Cells.
Article in Oncology research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Triple-negative breast cancer (TNBC) is an aggressive subtype with poor prognosis and resistance to conventional therapies, including radiotherapy. Cancer stem cells (CSCs) drive tumor initiation, metastasis, and therapy resistance in TNBC. Identifying pathways sustaining CSCs in radioresistant TNBC is key for targeted therapies. This study examines SRC proto-oncogene (SRC) and the signal transducer and activator of transcription 3 (STAT3) activation in radioresistance and CSC maintenance. Methods: A radioresistant MDA-MB-231 TNBC cell line (231RR) was developed and compared to the parental line for CSC activity and self-renewal. Western blotting assessed molecular changes; functional assays followed SRC and STAT3 inhibitor treatment. SRCY Results: 231RR cells exhibited enhanced CSC traits and upregulated SRC/STAT3 signaling, with heightened sensitivity to SRC/STAT3 inhibitors. Forced expression of SRCY530F in parental cells boosted STAT3 activation and CSC activity. SRC/STAT3 inhibition reduced HK2 without impairing glycolysis. HK2 knockdown decreased MYC proto-oncogene (c-MYC) and octamer-binding transcription factor-4 (OCT4). Finally, the suppression of epidermal growth factor receptor (EGFR) activation by gefitinib resulted in the inhibition of the SRC/STAT3/HK2 axis. TCGA data linked SRC to glycolytic signatures in breast cancer. Conclusions: The EGFR/SRC/STAT3/HK2 axis drives radioresistance and CSC maintenance in TNBC via HK2 upregulation. HK2 promotes stemness mainly through non-metabolic means, not broad metabolic shifts. Targeting this pathway could overcome radioresistance and enhance TNBC outcomes.
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