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目的:研究解毒祛瘀方对人乳腺癌细胞侵袭能力的影响及机制。方法:以人乳腺癌MCF-7细胞为研究对象,预培养后分为空白组,解毒祛瘀方低、中、高剂量组(0.625,1.25,2.50 g·L-1),阳性药组(5-氟尿嘧啶,10 mg·L-1),分别用0.625,1.25,2.50 g·L-1的解毒祛瘀方及5-氟尿嘧啶处理人乳腺癌MCF-7细胞24 h后,MTT法检测细胞黏附率,Transwell小室实验检测细胞侵袭能力,RT-PCR法检测肿瘤细胞CD44,E-钙黏蛋白及N-钙黏蛋白基因的表达,Western blot法检测肿瘤细胞CD44,E-钙黏蛋白,N-钙黏蛋白,磷酸化细胞外信号调节激酶(p-ERK)及磷酸化蛋白激酶B(p-Akt)蛋白的表达。结果:与空白组比较,解毒祛瘀方低、中、高剂量组可明显抑制人乳腺癌MCF-7细胞的黏附和侵袭能力;且使CD44及E-钙黏蛋白基因及蛋白表达上调,N-钙黏蛋白表达下调,并可以抑制PI3K/Akt及MEK/ERK信号通路的激活(P<0.05,P<0.01)。结论:解毒祛瘀方可抑制人乳腺癌MCF-7细胞体外侵袭能力,其机制可能与抑制相关异质黏附蛋白的表达、抑制上皮间质转化及调节肿瘤相关信号通路有关。
Objective: To study the effect and mechanism of Jiedu Quyu Prescription on invasion of human breast cancer cells. Methods: Human breast cancer MCF-7 cells were divided into blank group, low, medium and high dose groups (0.625,1.25,2.50 g · L-1) 5-fluorouracil, 10 mg · L-1). The human breast cancer MCF-7 cells were treated with 0.625,1.25,2.50 g · L-1 detoxification and stasis-removing prescription and 5-fluorouracil for 24 h, The cell invasive ability was detected by Transwell chamber assay. The expression of CD44, E-cadherin and N-cadherin gene were detected by RT-PCR. The expressions of CD44, E-cadherin, Cadherin, phosphorylated extracellular signal-regulated kinase (p-ERK) and phosphorylated protein kinase B (p-Akt) protein expression. Results: Compared with the blank group, Jiedu Quyu Fang low, medium and high dose groups can significantly inhibit the adhesion and invasion ability of human breast cancer MCF-7 cells; and up-regulate the expression of CD44 and E-cadherin genes and proteins, N - cadherin expression was down - regulated, and the activation of PI3K / Akt and MEK / ERK signaling pathways were inhibited (P <0.05, P <0.01). Conclusion: Jiedu Quyu can inhibit the invasiveness of human breast cancer MCF-7 cells in vitro. The mechanism may be related to the inhibition of the expression of related adhesion molecules, the inhibition of epithelial-mesenchymal transition and the regulation of tumor-related signaling pathways.