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目的:探讨常春藤皂苷元(HG)通过调控上皮-间质转化(EMT)途径抑制大肠癌侵袭转移的机制。方法:以肠癌细胞SW480细胞为研究对象,不同质量浓度HG干预转化生长因子-β1(TGF-β1)诱导的SW480细胞,作用24 h后噻唑蓝(MTT)法检测细胞增殖能力。转移小室(Transwell)实验检测细胞侵袭能力。实时荧光定量-聚合酶链式反应(q PCR)和蛋白质免疫印迹(Western blot)法分别检测EMT标志物E-钙黏蛋白(E-cadherin),N-钙黏蛋白(N-cadherin),波形蛋白(Vimentin),蜗牛同源物1(果蝇)样1蛋白(Snail)及侵袭转移标志分子信号传导蛋白和转录激活物(STAT3),基质金属蛋白酶-9(MMP-9),MMP~(-1)4,伴有Kazal域的富含半胱氨酸的逆转诱导蛋白(RECK)表达变化。结果:HG可抑制TGF-β1诱导的肠癌SW480细胞增殖、干预EMT和降低侵袭能力,降低EMT标志分子N-cadherin,Vimentin,Snail及侵袭转移标志分子STAT3,MMP-9,MMP~(-1)4表达,增强E-cadherin,RECK的表达,与TGF-β1组比较均具有统计学差异(P<0.05)。结论:HG可通过抑制EMT途径影响大肠癌细胞SW480侵袭转移。
Objective: To investigate the mechanism by which hederagenin (HG) inhibits the invasion and metastasis of colorectal carcinoma by regulating epithelial-mesenchymal transition (EMT) pathway. Methods: Human colorectal cancer cell line SW480 was treated with different concentrations of HG. TGF-β1-induced SW480 cells were treated with different concentrations of HG for 24 h. Cell proliferation was measured by MTT assay. Transwell assay was used to detect cell invasion. The expression of EMT markers E-cadherin, N-cadherin, waveforms were detected by qPCR and Western blotting respectively. Vimentin, Snail, STAT1, MMP-9, MMP-9, MMP-9, -1) 4, cysteine-associated reverse transcription-inducing protein (RECK) with Kazal domain. Results: HG could inhibit the proliferation of SW480 cells induced by TGF-β1, the intervention of EMT and the decrease of invasiveness, and the decrease of EMT markers N-cadherin, Vimentin, Snail and STAT3, MMP-9 and MMP- ) 4 expression, enhanced E-cadherin, RECK expression, compared with the TGF-β1 group were statistically significant (P <0.05). Conclusion: HG can affect the invasion and metastasis of colorectal cancer cell line SW480 by inhibiting the EMT pathway.