Triple-negative breast cancer (TNBC) is a subtype breast cancer with aggressive behavior, advanced disease status and poor prognosis. Because of the lack of targeting agents and limited therapeutic options, treatment of TNBC remains a great clinical challenge. Vasohibin 2 (VASH2) was previously identified as an angiogenic factor, but its role in TNBC tumorigenesis is unknown. Using quantitative PCR and western blot analyses, we found that VASH2 is overexpressed in TNBC cells and tissues. Knockdown of VASH2 via siRNA inhibited the proliferation of the TNBC cell lines by delaying cell cycle progression and increasing apoptosis. Further analyses showed that the VASH2-mediated increase in the transcription of fibroblast growth factor-2, vascular endothelial growth factor and vasohibin 1 may be the mechanism underlying these effects. Taken together, these data indicate that VASH2 is abnormally expressed in TNBC, indicating a novel and important role for VASH2 in TNBC malignant transformation.
Keywords: TNBC; VASH2; cell cycle; invasion; proliferation.