关键词: SRPK1、 PI3K、 生长、 AKT、 三阴性乳腺癌、 凋亡、 侵袭、 进展

Abstract: Objective To explore the role of SRPK1 and PI3K / AKT signaling pathway in themalignant progression of triple negative breast cancer ( TNBC) cells. Methods The expressionlevel of SRPK1 in TNBC tissues and adjacent tissues was detected by immunohistochemistry. TNBCcell line MDA-MB-231 cells were divided into three groups: siSRPK1 group, siNC group andLY294002 group. The proliferation ability of MDA-MB-231 cells was detected by MTT assay. Transwell assay was used to analyze the invasion ability of MDA-MB-231 cells. The apoptosis rate of MDA-MB-231 cells was analyzed by flow cytometry. The expression of PI3K / AKT signalingpathway related proteins and SRPK1 protein were detected by Western blotting. Results The expression level of SRPK1 was increased in the TNBC tissues when compared with that in the adjacenttissues. The growth rates of MDA-MB-231 cells in the siSRPK1 and LY294002 groups were decreased when compared with that in the siNC group (P < 0. 05). The numbers of invasive MDA-MB- 231 cells in the siSRPK1 and LY294002 groups were significantly decreased (P < 0. 05). The apoptosis rates of MDA-MB-231 cells in the siSRPK1 and LY294002 groups were significantly increased (P< 0. 05). The protein expression levels of PI3K and AKT in MDA-MB-231 cells were significantly decreased in the siSRPK1 and LY294002 groups ( P < 0. 05). Conclusion SRPK1 is highly expressed in TNBC tissues. After inhibiting the expression of SRPK1, the proliferation and invasion ability of TNBC MDA-MB-231 cells are decreased, and the apoptosis rate is increased. This process is related to the regulation of SRPK1 on PI3K / AKT pathway.

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