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Downregulation of TSPAN1 inhibits angiogenesis in triple-negative breast cancer cells by regulating the PI3K/Akt signaling pathway
1Department of Pathology, Pingshan District People’s Hospital, 518100 Shenzhen, Guangdong, China
DOI: 10.22514/ejgo.2025.122 Vol.46,Issue 9,September 2025 pp.71-76
Submitted: 20 May 2025 Accepted: 21 July 2025
Published: 15 September 2025
*Corresponding Author(s): Yange Wu E-mail: ygwu6153@163.com
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.
Triple-negative breast cancer; TSPAN1; PI3K/Akt; Angiogenesis
Yange Wu,Wenxiu Chen,Jing Zhang. Downregulation of TSPAN1 inhibits angiogenesis in triple-negative breast cancer cells by regulating the PI3K/Akt signaling pathway. European Journal of Gynaecological Oncology. 2025. 46(9);71-76.
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