Downregulation of TSPAN1 inhibits angiogenesis in triple-negative breast cancer cells by regulating the PI3K/Akt signaling pathway

Background: Triple-negative breast cancer (TNBC) progression and invasion highly depends on abnormal angiogenesis. While tetraspanin 1 (TSPAN1) has been implicated in the malignant progression of TNBC, its relationship in tumor angiogenesis remains poorly understood. Methods: Tumor samples were collected from patients with TNBC and analyzed using clinical pathological and Western blot analyses. TSPAN1 expression was knocked down in the TNBC cell line, Hs-578T using siRNA technology. The angiogenic ability of human umbilical vein endothelial cells (HUVECs) was evaluated by lumen formation assay. The Phosphatidylinositol 3-Kinase (PI3K)/Protein Kinase B (Akt) signaling pathway was detected using western blots. Results: TSPAN1 overexpression in TNBC tumors is linked to metastasis and PI3K/Akt pathway activation. Knockdown of TSPAN1 in TNBC cells, significantly suppressed the tube formation ability of co-cultured HUVECs. Mechanistically, TSPAN1 knockdown significantly inhibited the activity of the PI3K/Akt pathway. Conclusions: In conclusion, TSPAN1 promotes TNBC angiogenesis via activation of PI3K/Akt signaling pathway.