医学分子生物学杂志2024，Vol.21Issue(2)：161-165,5.DOI:10.3870/j.issn.1672-8009.2024.02.011
SRPK1激活PI3K/AKT通路对三阴性乳腺癌细胞恶性进展的影响
Effect of SRPK1 on Malignant Progression of Triple Negative Breast Cancer Cells by Activation of the PI3K/AKT Pathway
摘要
Abstract
Objective To explore the role of SRPK1 and PI3K/AKT signaling pathway in the malignant progression of triple negative breast cancer(TNBC)cells.Methods The expression level of SRPK1 in TNBC tissues and adjacent tissues was detected by immunohistochemistry.TNBC cell line MDA-MB-231 cells were divided into three groups:si SRPK1 group,siNC group and LY294002 group.The proliferation ability of MDA-MB-231 cells was detected by MTT as-say.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 signaling pathway related proteins and SRPK1 protein were detected by Western blotting.Results The ex-pression level of SRPK1 was increased in the TNBC tissues when compared with that in the adjacent tissues.The growth rates of MDA-MB-231 cells in the si SRPK1 and LY294002 groups were de-creased when compared with that in the siNC group(P<0.05).The numbers of invasive MDA-MB-231 cells in the si SRPK1 and LY294002 groups were significantly decreased(P<0.05).The apop-tosis rates of MDA-MB-231 cells in the si SRPK1 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 si SRPK1 and LY294002 groups(P<0.05).Conclusion SRPK1 is highly ex-pressed in TNBC tissues.After inhibiting the expression of SRPK1,the proliferation and invasion a-bility 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.关键词
SRPK1/PI3K/生长/AKT/三阴性乳腺癌/凋亡/侵袭/进展Key words
SRPK1/PI3K/growth/AKT/triple negative breast cancer/apoptosis/inva-sion/progression分类
医药卫生引用本文复制引用
姜丽,王慧慧,柯龙珠,李功卓,罗莉..SRPK1激活PI3K/AKT通路对三阴性乳腺癌细胞恶性进展的影响[J].医学分子生物学杂志,2024,21(2):161-165,5.基金项目
贵州省卫生健康委科学技术基金(No.gzwkj2021-061,No.gzwkj2021-060),贵州省中医药管理局中医药、民族医药科学技术研究课题(No.QzYY-2023-009) This work was supported by grants from the Guizhou Health Commission Science and Technology Program(No.gzwkj2021-061,No.gzwkj2021-060),Guizhou Administration of Traditional Chinese Medicine Research Program(No.QzYY-2023-009) （No.gzwkj2021-061,No.gzwkj2021-060）
