ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026
KCTD15 Enhances Stem Cell-Like Properties and Promotes Triple-Negative Breast Cancer Progression Through KLF4/β-Catenin Signaling.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- A Global Analysis of the Complex Structural Organization of KCTD Proteins and Their Functional Implications.International journal of molecular sciences · 2026Review
- KCTD15 Enhances Stem Cell-Like Properties and Promotes Triple-Negative Breast Cancer Progression Through KLF4/β-Catenin Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
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Authors and funding
4 authors.
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Abstract
Triple-negative breast cancer (TNBC) remains an aggressive malignancy with limited therapeutic options and poor prognosis, underscoring the critical need for novel therapeutic targets. This investigation elucidates the functional role of the potassium channel tetramerization domain 15 (KCTD15) in TNBC progression, providing mechanistic insights into its potential as a therapeutic target for this challenging disease. KCTD15 exhibited high expression in TNBC tissues, correlating with advanced grade and unfavorable prognosis. Functionally, KCTD15 knockdown in TNBC cell lines (BT-549/MDA-MB-231) markedly suppressed cellular proliferation, migration, and cancer stem cell properties, while concomitantly enhancing apoptosis. Mechanistically, KCTD15 directly interacted with KLF4, facilitating its nuclear translocation and subsequent activation of the β-catenin signaling cascade. Notably, KLF4 knockdown abrogated KCTD15-mediated stemness maintenance and β-catenin pathway activation. In vivo, KCTD15 silencing reduced xenograft tumor growth and downregulated Ki67, KLF4, and β-catenin protein expression in tumor tissues, confirming its oncogenic role through the KLF4/β-catenin axis. Our findings establish KCTD15 as a pivotal regulator of TNBC stemness through modulation of the KLF4/β-catenin signaling axis. These results provide a robust preclinical rationale for developing therapeutic strategies targeting this molecular axis in TNBC management.
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