【摘要】：目的探討鼠尾草酸聯(lián)合他莫昔芬對(duì)乳腺癌細(xì)胞的影響及作用機(jī)制。方法將乳腺癌細(xì)胞株MCF-7、T47D分為4組,對(duì)照組加入PBS,CA組加入鼠尾草酸,TAM組加入他莫昔芬,CA+TAM組加入鼠尾草酸和他莫昔芬。MTT增殖實(shí)驗(yàn)檢測(cè)細(xì)胞增殖能力,集落形成實(shí)驗(yàn)檢測(cè)細(xì)胞集落形成能力,Transwell小室實(shí)驗(yàn)檢測(cè)細(xì)胞侵襲能力,細(xì)胞劃痕實(shí)驗(yàn)檢測(cè)細(xì)胞遷移能力,免疫印跡法檢測(cè)各組細(xì)胞Caspase-8、Caspase-3、PARP蛋白表達(dá)。結(jié)果在0~20μmol/L藥物濃度時(shí),CA、TAM、CA+TAM呈劑量依賴性抑制乳腺癌細(xì)胞增殖,但藥物濃度為20μmol/L與50μmol/L對(duì)細(xì)胞增殖影響差異無(wú)統(tǒng)計(jì)學(xué)意義(均P0.05)。CA+TAM組增殖抑制率明顯高于CA組和TAM組(均P0.05)。MCF-7和T47D細(xì)胞中,CA組、TAM組、CA+TAM組集落形成率、侵襲細(xì)胞數(shù)、細(xì)胞遷移率顯著低于對(duì)照組(均P0.05);CA+TAM組集落形成率、侵襲細(xì)胞數(shù)、細(xì)胞遷移率顯著低于CA組和TAM組(均P0.05),CA組和TAM組集落形成率、侵襲細(xì)胞數(shù)、細(xì)胞遷移率比較差異均無(wú)統(tǒng)計(jì)學(xué)意義(均P0.05)。在2種乳腺癌細(xì)胞株中,對(duì)照組、CA組、TAM組、CA+TAM組cleaved Caspase-8蛋白表達(dá)差異無(wú)統(tǒng)計(jì)學(xué)意義(均P0.05),CA組、TAM組、CA+TAM組cleaved Caspase-3、cleaved PARP蛋白表達(dá)顯著高于對(duì)照組(均P0.05),CA+TAM組cleaved Caspase-3、cleaved PARP蛋白表達(dá)顯著高于CA組和TAM組(均P0.05),CA組和TAM組cleaved Caspase-3、cleaved PARP蛋白表達(dá)差異無(wú)統(tǒng)計(jì)學(xué)意義(均P0.05)。結(jié)論鼠尾草酸聯(lián)合他莫昔芬能夠抑制乳腺癌細(xì)胞的增殖、遷移和侵襲,其作用機(jī)制可能與激活Caspase-3/PARP信號(hào)通路有關(guān)。
[Abstract]:Objective to investigate the effect and mechanism of salicylic acid combined with tamoxifen on breast cancer cells. Methods Breast cancer cell line MCF-7,T47D was divided into four groups. The control group was added with PBS,CA group and the TAM group was added with tamoxifen, CA TAM group. The proliferation ability of the cells was measured by MTT proliferation assay. Colony forming assay was used to detect cell colony formation ability, Transwell chamber assay to detect cell invasion ability, cell scratch assay to detect cell migration ability, and Western blot method to detect the expression of Caspase-8,Caspase-3,PARP protein. Results at 0 渭 mol/L concentration, CA,TAM,CA TAM inhibited the proliferation of breast cancer cells in a dose-dependent manner. However, there was no significant difference between 20 渭 mol/L and 50 渭 mol/L in cell proliferation (P 0.05). The inhibitory rate of proliferation in). CA TAM group was significantly higher than that in CA group and TAM group (P0.05). The colony formation rate, number of invading cells and cell migration rate in CA TAM group were significantly lower than those in control group (P0.05). The colony formation rate, invasive cell number and cell migration rate in CA TAM group were significantly lower than those in CA group and TAM group (P0.05). There was no significant difference in colony formation rate, invasive cell number and cell migration rate between), CA group and TAM group (P0.05). There was no significant difference in the expression of cleaved Caspase-8 protein among two breast cancer cell lines, control group, CA group, TAM group and, CA TAM group (P0.05 in), CA group, cleaved Caspase-3, in, CA TAM group in TAM group). The expression of cleaved PARP protein was significantly higher in), CA TAM group than in control group (P0.05). The expression of cleaved Caspase-3,cleaved PARP protein in), CA TAM group was significantly higher than that in CA group and TAM group (P0.05 in), CA group and TAM group). There was no significant difference in the expression of cleaved PARP protein (P0.05). Conclusion Salmonic acid combined with tamoxifen can inhibit the proliferation, migration and invasion of breast cancer cells, and its mechanism may be related to the activation of Caspase-3/PARP signaling pathway.
【作者單位】： 華中科技大學(xué)同濟(jì)醫(yī)學(xué)院附屬武漢市中心醫(yī)院中西醫(yī)結(jié)合腫瘤科;
【分類號(hào)】：R737.9

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