SRPK1激活PI3K/AKT通路对三阴性乳腺癌细胞恶性进展的影响OACSTPCD
Effect of SRPK1 on Malignant Progression of Triple Negative Breast Cancer Cells by Activation of the PI3K/AKT Pathway
目的 探索SRPK1 与PI3K/AKT途径在三阴性乳腺癌恶性进展中的作用.方法 免疫组化实验检测三阴性乳腺癌组织以及癌旁组织SRPK1 的表达水平;将三阴性乳腺癌细胞系MDA-MB-231 细胞分为 3个实验组:si SRPK1 组、siNC组以及LY294002 组.通过MTT实验检测MDA-MB-231 细胞的增殖能力;通过Transwell实验分析MDA-MB-231 细胞的侵袭能力;通过流式细胞术分析MDA-MB-231 细胞的凋亡率;通过蛋白免疫印迹检测PI3K/AKT信号通路以及SRPK1 蛋白的表达水平.结果 和三阴性乳腺癌的癌旁组织比较,三阴性乳腺癌组织SRPK1 的表达水平增加.与siNC组比较,si SRPK1 以及LY294002 组的MDA-MB-231 细胞增殖能力下降(P<0.05);si SRPK1 以及LY294002 组的MDA-MB-231 细胞侵袭数减少(P<0.05);si SRPK1 以及LY294002 组的MDA-MB-231 细胞凋亡率升高(P<0.05);si SRPK1 以及LY294002 组的MDA-MB-231 细胞PI3K、AKT蛋白水平降低(P<0.05).结论 SRPK1 在三阴性乳腺癌组织中高表达,抑制SRPK1 表达后,三阴性乳腺癌MDA-MB-231 细胞的增殖以及侵袭能力降低,凋亡率增加,这一过程与SR-PK1 调控PI3K/AKT通路相关.
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.
姜丽;王慧慧;柯龙珠;李功卓;罗莉
联勤保障部队第970医院肿瘤科 山东省烟台市,264002湖北中医药大学中医临床学院 武汉市,430070贵航贵阳医院肿瘤科 贵阳市,550027
临床医学
SRPK1PI3K生长AKT三阴性乳腺癌凋亡侵袭进展
SRPK1PI3KgrowthAKTtriple negative breast cancerapoptosisinva-sionprogression
《医学分子生物学杂志》 2024 (002)
161-165 / 5
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)
评论