發(fā)布時(shí)間：2018-06-22 19:59

  本文選題：微小RNA + 肝細(xì)胞癌　； 參考：《中國藥理學(xué)通報(bào)》2017年05期

【摘要】：目的探討微小RNA155(microRNA-155,miR-155)在肝細(xì)胞癌(hepatocellular carcinoma,HCC)對(duì)索拉非尼(sorafenib)抗藥中的作用。方法將miR-155抑制慢病毒(miR-155 inhibitor)轉(zhuǎn)染miR-155表達(dá)相對(duì)較高的SMMC-7721細(xì)胞,而miR-155過表達(dá)慢病毒(miR-155)轉(zhuǎn)染miR-155表達(dá)相對(duì)較低的Hep G2細(xì)胞;用熒光定量PCR(qPCR)檢測(cè)經(jīng)慢病毒轉(zhuǎn)染的SMMC-7721細(xì)胞及HepG2細(xì)胞miR-155表達(dá)量,以驗(yàn)證慢病毒轉(zhuǎn)染效果;通過CCK-8法及流式細(xì)胞術(shù)檢測(cè)各組細(xì)胞經(jīng)索拉非尼作用后的存活率及凋亡情況;用Western blot檢測(cè)凋亡相關(guān)蛋白活性caspase-3表達(dá)量,從而進(jìn)一步探究各組細(xì)胞凋亡情況。結(jié)果與對(duì)照組相比,轉(zhuǎn)染miR-155抑制慢病毒的SMMC-7721細(xì)胞表達(dá)miR-155明顯下調(diào)(P0.01),經(jīng)索拉非尼處理后其存活率明顯降低(P0.05),而索拉非尼誘導(dǎo)其凋亡明顯增加(P0.01),其活性caspase-3表達(dá)量明顯上調(diào)(P0.01);miR-155過表達(dá)慢病毒轉(zhuǎn)染HepG2細(xì)胞后,則相反。結(jié)論 miR-155參與肝細(xì)胞癌對(duì)索拉非尼的抗藥,有希望成為一個(gè)肝癌治療的新靶標(biāo)。
[Abstract]:Objective to investigate the role of microRNA-155 miR-155 in the resistance of hepatocellular carcinoma to Solafenil (sorafenib). Methods miR-155 inhibited lentivirus (miR-155 inhibitor) was transfected into SMMC-7721 cells with relatively high miR-155 expression, while miR-155 overexpression lentivirus (miR-155) was transfected into Hep G2 cells with relatively low miR-155 expression. The expression of miR-155 in SMMC-7721 cells and HepG2 cells was detected by fluorescence quantitative polymerase chain reaction (qPCR). In order to verify the effect of lentivirus transfection, CCK-8 and flow cytometry were used to detect the survival rate and apoptosis of the cells treated with Solafenil, and Western blot was used to detect the expression of apoptosis-related protein (caspase-3). So as to further explore the apoptosis of each group. Results compared with the control group, The expression of miR-155 was down-regulated (P0.01) in SMMC-7721 cells transfected with miR-155. The survival rate of SMMC-7721 cells treated with sorafenil was significantly decreased (P0.05), while the apoptosis induced by sorafenil was significantly increased (P0.01). The expression of active caspase-3 was up-regulated (P0.01) and the overexpression of miR-155 was up-regulated (P0.01) in HepG2 cells. The opposite is true. Conclusion miR-155 may be a new target for the treatment of hepatocellular carcinoma.
【作者單位】： 重慶醫(yī)科大學(xué)附屬第一醫(yī)院肝膽外科;
【基金】：國家自然科學(xué)基金資助項(xiàng)目(No 81470898)
【分類號(hào)】：R735.7

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