Kisspeptin 10 reactivates KISS1, suppresses metastasis, and promotes apoptosis in triple-negative breast cancer

Triple-negative breast cancer is an aggressive subtype lacking ER, PR, and HER2 receptors, making it highly clinically challenging. In MDA-MB-231 and MDA-MB-468 cells. Kisspeptin 10 (Kp-10) treatment significantly reduced cell viability and migration and induced a dose-dependent upregulation of KISS1 mRNA, suggesting a positive feedback loop.  Kp-10 also modulated key transcription factors — upregulating GATA2, CDX2, and FLI1 while downregulating ZEB1 — indicating a shift towards a less aggressive transcriptional state.  EMT reversal was evident from increased E-cadherin and β-catenin, and reduced N-cadherin, CD44, and Vimentin. Pro-apoptotic genes CASP3, CASP8, CASP9, and BAX were upregulated, while BCL2 was suppressed, suggesting activation of both apoptotic pathways.  Metabolomics profiling showed changes in pathways related to apoptosis, anti-angiogenesis, and redox homeostasis. In silico analysis confirmed reduced KISS1 expression in metastatic TNBC tissues and showed a correlation between high GATA2/CASP9 levels and improved survival.  Kisspeptin-10 reactivates KISS1 and induces anti-tumour effects via transcriptional, apoptotic, and metabolic reprogramming, demonstrating its potential as a therapeutic agent in triple-negative breast cancer.

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