首页|双歧杆菌完整肽聚糖对结肠癌细胞SW480株PI3K/AKT信号通路关键因子作用机制

双歧杆菌完整肽聚糖对结肠癌细胞SW480株PI3K/AKT信号通路关键因子作用机制

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目的 探讨完整肽聚糖(whole peptidoglycan,WPG)对人结肠癌细胞系SW480的上皮间质转化(EMT)作用与机制。方法 实验分为3组:对照组(SW480结肠癌细胞)、EMT组(TGF-β1诱导组)和EMT+WPG组(TGF-β1诱导后加入WPG);采用CCK-8法检测各组细胞的增殖能力;划痕实验检测各组细胞的迁移能力;Transwell实验检测各组细胞的侵袭能力;Western Blot法检测p-PI3K/PI3K、p-AKT/AKT、Vimentin和E-cadherin蛋白的表达;流式细胞术检测各组细胞的凋亡。结果 TGF-β1诱导人结肠癌细胞SW480的EMT发生(P<0。0500),TGF-β1 诱导 EMT组的增殖能力(t=0。795 3,P=0。4494)、迁移能力(t=1。289 0,P=0。2670)及侵袭能力(t=7。583 0,P<0。000 1)均高于对照组;而EMT+WPG组的增殖能力(t=3。665 0,P=0。0064)、迁移能力(t=5。1210,P=0。0069)及侵袭能力(t=7。7110,P=0。000 1)均低于TGF-β1诱导EMT组。与对照组相比,TGF-β1 诱导 EMT 组中 p-PI3K/PI3K(t=5。785 0,P=0。004 4)、p-AKT/AKT(t=1。128 0,P=0。007 1)、Vimentin(t=3。339 0,P=0。002 4)表达均增加,E-钙黏蛋白的相对表达减少(t=4。8540,P=0。008 3);而EMT+WPG组中 p-PI3K/PI3K(t=4。131 0,P=0。000 2)、p-AKT/AKT(t=3。721 0,P=0。033 7)、Vimentin(t=1。756 0,P=0。091 0)蛋白表达较TGF-β1诱导EMT组均降低,E-钙黏蛋白的相对表达增加(t=1。6450,P=0。115 0),且细胞凋亡增多(t=13。400 0,P=0。000 2)。结论 WPG通过调控PI3K/AKT信号抑制结肠癌细胞系SW480的EMT进而抑制结肠癌细胞的侵袭转移。
Mechanism of action of Bifidobacteria on PI3K/AKT signaling pathway in SW480 strain of colon cancer cells
Objective To explore the effect and mechanism of whole peptidoglycan(WPG)in epithelial stromal trans-formation(EMT)in the human colon cancer cell line SW480.Methods Three groups were designed:control group(SW480 colon cancer cells),EMT group(TGF-β1 induction group)and EMT+WPG group(WPG was added after TGF-β1 induction).The proliferative capacity of the cells in each group was determined with CCK-8 assay;the scratch experiment to detect the migration ability of the cells;and Transwell to determine the invasion ability of each group of cells.The ex-pressions of p-PI3K/PI3K,p-AKT/AKT,Vimentin,and E-cadherin proteins were detected using Western Blot;apoptosis of the cells was determined using flow cytometry.Results TGF-β1 induced EMT of SW480 in human colon cancer cells(P<0.050 0).Higher proliferation(t=0.795 3,P=0.449 4),migration(t=1.289 0,P=0.267 0)and invasion(t=7.583 0,P<0.000 1)were seen in TGF-β1 induced EMT group than in controls,while the proliferation(t=3.665 0,P=0.006 4),mi-gration(t=5.121 0,P=0.006 9)and invasion(t=7.711 0,P=0.000 1)in EMT+WPG group were lower than in TGF-β1-in-duced EMT group.The expression of p-PI3K/PI3K(t=5.785 0,P=0.004 4),p-AKT/AKT(t=1.128,P=0.007 1)and Vi-mentin(t=3.339 0,P=0.002 4)in TGF-β1 induced EMT groups increased compared with control group,while that of E-cadherin reduced(t=4.854 0,P=0.008 3);the difference was statistically significant.The expressions of p-PI3K/PI3K(t=4.131 0,P=0.000 2),p-AKT/AKT(t=3.721 0,P=0.033 7)and Vimentin(t=1.756 0,P=0.091 0)were lower in EMT+WPG group than in TGF-β1 induced EMT group,while that of E-cadherin increased(t=1.645 0,P=0.115 0),and cell apoptosis increased(t=13.400 0,P=0.000 2);the difference was statistically significant.Conclusion WPG inhibited the epithelial stromal transformation of colon cancer cell line SW480 and then inhibited the invasion and metastasis of colon cancer cells through regulating PI3K/AKT signaling pathway.

Whole peptidoglycanSW480 cell lineEpithelial stromal transitionInvasion and metastasis

王伟杰、谢小亮、周洁、宋伟、马硕、李海

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宁夏医科大学总医院结直肠外科,宁夏银川 750000

完整肽聚糖 SW480细胞系 上皮间质转化 侵袭和转移

宁夏回族自治区自然科学基金

2022AAC03571

2024

中国微生态学杂志
中华预防医学会 大连医科大学

中国微生态学杂志

CSTPCD北大核心
影响因子:1.115
ISSN:1005-376X
年,卷(期):2024.36(5)