本文關鍵詞：miR-183在子宮內膜癌Ishikawa細胞中的表達及其對p53蛋白的調節(jié)作用　出處：《中國婦幼保健》2016年24期 　論文類型：期刊論文

  更多相關文章： 子宮內膜癌 Ishikawa細胞 miR- p蛋白

【摘要】：目的探討miR-183在子宮內膜癌Ishikawa細胞中的表達及其對p53蛋白表達和細胞增殖、凋亡的影響。方法采用LipofectaminerTM2000脂質體將miR-183的特異性抑制劑反義寡核苷酸轉染到Ishikawa細胞(實驗組),不相關序列、脂質體和未轉染組細胞分別為陰性對照組、脂質體對照組和空白對照組。采用CCK-8法和流式細胞儀分別檢測各組子宮內膜癌Ishikawa細胞的增殖和凋亡情況;采用RT-PCR檢測miR-183和p53 mRNA在各組子宮內膜癌Ishikawa細胞中的表達水平;采用Western blot檢測p53蛋白在各組子宮內膜癌Ishikawa細胞中的表達水平。結果 CCK-8檢測結果顯示:轉染0~24 h,實驗組、空白對照組、脂質體對照組子宮內膜癌Ishikawa細胞增速相似,陰性對照組子宮內膜癌Ishikawa細胞增速略快;轉染24~48 h,實驗組、空白對照組和脂質體對照組子宮內膜癌Ishikawa細胞增速較快;轉染48~72 h,實驗組子宮內膜癌Ishikawa細胞較其余3組增長速度快;轉染72~96 h,4組子宮內膜癌Ishikawa細胞繼續(xù)保持增長狀態(tài),且達到對數生長期,實驗組子宮內膜癌Ishikawa細胞較其余3組增速快。流式細胞學檢測結果顯示:轉染3 d后,實驗組較其余3組早期凋亡率明顯降低,差異有統計學意義(P0.05);陰性對照組較其余3組早期凋亡率明顯增高,差異有統計學意義(P0.05)。RT-PCR結果顯示:實驗組miR-183表達水平明顯低于其余3組,差異有統計學意義(P0.05);實驗組p53 mRNA表達水平明顯低于其余3組,差異有統計學意義(P0.05)。Western blot檢測結果顯示:實驗組p53蛋白表達水平明顯高于其余3組,差異有統計學意義(P0.05)。結論 miR-183在子宮內膜癌Ishikawa細胞中有表達,miR-183抑制劑能有效抑制miR-183在子宮內膜癌Ishikawa細胞中的表達,促進細胞增殖,抑制細胞凋亡,上調p53蛋白表達。miR-183可能通過抑制p53蛋白表達而抑制子宮內膜癌細胞增殖,促進凋亡,從而影響子宮內膜癌的發(fā)生、發(fā)展及預后。
[Abstract]:Objective to investigate the expression of miR-183 in endometrial carcinoma Ishikawa cells and its expression of p53 protein and cell proliferation. Methods LipofectaminerTM2000 liposome was used to transfect antisense oligodeoxynucleotides (antisense oligonucleotides), a specific inhibitor of miR-183, into Ishikawa cells. Experimental group). Unrelated sequences, liposomes and untransfected cells were respectively negative control group. CCK-8 assay and flow cytometry were used to detect the proliferation and apoptosis of endometrial carcinoma Ishikawa cells in each group. RT-PCR was used to detect the expression of miR-183 and p53 mRNA in Ishikawa cells of endometrial carcinoma. Western blot was used to detect the expression of p53 protein in Ishikawa cells of endometrial carcinoma. Results the results of CCK-8 assay showed that the expression of p53 protein was 0 24 h after transfection. In experimental group, blank control group and liposome control group, the growth rate of Ishikawa cells in endometrial carcinoma was similar, while that in negative control group was a little faster. After transfection for 24 ~ 48 h, the growth rate of Ishikawa cells in experimental group, blank control group and liposome control group was higher than that in control group. After transfection for 48 ~ 72 h, the Ishikawa cells of endometrial carcinoma in the experimental group increased faster than those in the other three groups. The Ishikawa cells of endometrial carcinoma in 72 ~ 96 h after transfection continued to increase and reached the logarithmic growth stage. The growth rate of Ishikawa cells in the experimental group was faster than that in the other three groups. The results of flow cytometry showed that the apoptosis rate of the experimental group was significantly lower than that of the other three groups after 3 days of transfection. The difference was statistically significant (P 0.05). The rate of apoptosis in the negative control group was significantly higher than that in the other three groups, and the difference was statistically significant. The results of RT-PCR showed that the expression of miR-183 in the experimental group was significantly lower than that in the other three groups. The difference was statistically significant (P 0.05). The expression of p53 mRNA in the experimental group was significantly lower than that in the other three groups. The expression of p53 protein in the experimental group was significantly higher than that in the other three groups. Conclusion miR-183 is expressed in Ishikawa cells of endometrial carcinoma. MiR-183 inhibitor can effectively inhibit the expression of miR-183 in endometrial carcinoma Ishikawa cells, promote cell proliferation and inhibit cell apoptosis. Upregulating the expression of p53 protein .miR-183 may inhibit the proliferation of endometrial carcinoma cells and promote apoptosis by inhibiting the expression of p53 protein, thus affecting the occurrence, development and prognosis of endometrial carcinoma.
【作者單位】： 河北醫(yī)科大學第三醫(yī)院婦產科;伊犁哈薩克自治州友誼醫(yī)院婦產科;
【分類號】：R737.33
【正文快照】： 子宮內膜癌是女性生殖系統常見惡性腫瘤之一,嚴重影響女性的健康和生命。隨著分子生物學技術的發(fā)展,研究者們發(fā)現p53基因可能是子宮內膜癌發(fā)生、發(fā)展的重要基因,正常p53基因的缺失或突變可導致細胞無限生長,是腫瘤發(fā)生的一個早期事件。在人類惡性腫瘤患者中,至少50%的患者發(fā)生

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