A systematic study of Girdin on cell proliferation, migration and angiogenesis in different breast cancer subtypes

Breast cancer has one of the highest incidences in females worldwide. Girdin is a novel actin‑binding protein, that induces cell migration and angiogenesis. However, a systematic study of Girdin function in distinct subtypes of breast cancer has not been reported to date. Therefore, the present study aimed to investigate the role of Girdin on cell proliferation, migration and angiogenesis in different subtypes of breast cancer. For this purpose, the breast epithelial MCF‑7, breast ductal T47D and breast metastatic MDA‑MB‑231 cancer cell lines were selected. Girdin small interfering RNA (siRNA) was transfected into MCF‑7, T47D and MDA‑MB‑231 cells. Girdin knockdown suppressed cell viability and migration in the different cancer cells tested. Girdin knockdown also suppressed mRNA expression of vascular endothelial growth factor (VEGF), and activation of phosphatidyl inositol 3‑kinase (PI3K) and RAC‑α serine/threonine‑protein kinase (Akt) in the subtypes tested. In conclusion, these data indicate that Girdin knockdown suppressed cell viability and migration and may suppress angiogenesis via the PI3K/Akt signaling pathway, in various breast cancers subtypes. The present study therefore suggests a role for Girdin as a novel therapeutic target for breast cancer, independent of subtype.