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- Title
CD93 regulates breast cancer growth and vasculogenic mimicry through the PI3K/AKT/SP2 signaling pathway activated by integrin β1.
- Authors
Hong Liu; Jianhui Zhang; Yanjun Zhao; Zhixiong Fan; Yongheng Yang; Yuanyuan Mao; Jingyuan Yang; Shungao Ma
- Abstract
In women, breast cancer (BC) accounts for 7%-10% of all cancer cases and is one of the most common cancers. To identify a new method for treating BC, the role of CD93 and its underlying mechanism were explored. MDA-MB-231 cells were used in this study and transfected with si-CD93, si-MMRN2, oe-CD93, si-integrin β1, or oe-SP2 lentivirus. After MDA-MB-231 cells were transfected with si-NC or si-CD93, they were injected into nude mice by subcutaneous injection at a dose of 5 × 106/mouse to construct a BC animal model. The expression of genes and proteins and cell migration, invasion and vasculogenic mimicry were detected by RT-qPCR, western blot, immunohistochemistry, immunofluorescence, Transwell, and angiogenesis assays. In pathological samples and BC cell lines, CD93 was highly expressed. Functionally, CD93 promoted the proliferation, migration, and vasculogenic mimicry of MDA-MB-231 cells. Moreover, CD93 interacts with MMRN2 and integrin β1. Knockdown of CD93 and MMRN2 can inhibit the activation of integrin β1, thereby inhibiting the PI3K/AKT/SP2 signaling pathway and inhibiting BC growth and vasculogenic mimicry. In conclusion, the binding of CD93 to MMRN2 can activate integrin β1, thereby activating the PI3K/AKT/SP2 signaling pathway and subsequently promoting BC growth and vasculogenic mimicry.
- Subjects
VASCULOGENIC mimicry; CELLULAR signal transduction; CANCER cell growth; BREAST cancer; TUMOR growth; INTEGRINS
- Publication
Journal of Biochemical & Molecular Toxicology, 2024, Vol 38, Issue 4, p1
- ISSN
1095-6670
- Publication type
Article
- DOI
10.1002/jbt.23688