Kisspeptin-10 Shows Promise Against Triple-Negative Breast Cancer by Suppressing Metastasis

Triple-negative breast cancer (TNBC) is a highly aggressive and challenging form of breast cancer, characterized by the absence of estrogen, progesterone, and HER2 receptors. This lack of common therapeutic targets makes TNBC resistant to many standard treatments, leading to poor prognosis and high rates of recurrence and metastasis. Current treatment options are often limited to chemotherapy, which can have severe side effects and varying efficacy, highlighting an urgent need for novel and targeted therapies. This study investigates the therapeutic potential of exogenous kisspeptin-10 as a multi-faceted agent to combat TNBC by inducing KISS1 expression, suppressing metastasis, and promoting apoptosis (programmed cell death).

Exogenous kisspeptin-10 significantly inhibited TNBC cell proliferation in a dose-dependent manner, achieving a 48% reduction at 1 µM compared to untreated controls (p<0.001). In the xenograft mouse model, kisspeptin-10 treatment led to a remarkable 62% decrease in primary tumor volume and a 78% reduction in the number of lung metastatic nodules compared to vehicle-treated mice (p<0.001). > The most critical finding was the 3.1-fold increase in endogenous KISS1 gene expression and a 2.7-fold increase in apoptotic markers (e.g., cleaved caspase-3 and Bax/Bcl-2 ratio) within treated tumors, directly demonstrating its pro-apoptotic and anti-metastatic mechanisms. Furthermore, kisspeptin-10 significantly modulated key proteins involved in metastasis, causing a 45% decrease in MMP-9 (a matrix metalloproteinase that degrades extracellular matrix) and a 55% increase in E-cadherin (a cell adhesion molecule) levels in tumor tissues (p<0.01).