miR-26a-5p通過靶向THAP2促進(jìn)子宮內(nèi)膜癌細(xì)胞凋亡
發(fā)布時間:2019-01-19 09:28
【摘要】:目的:研究miR-26a-5p靶向THAP2對子宮內(nèi)膜癌細(xì)胞凋亡的影響。方法:實(shí)時熒光定量RT-PCR法檢測子宮內(nèi)膜癌細(xì)胞中miR-26a-5p表達(dá)水平。構(gòu)建以慢病毒為載體的miR-26a-5p過表達(dá)和干擾質(zhì)粒,分別轉(zhuǎn)染子宮內(nèi)膜癌細(xì)胞系Ishikawa與KLE,實(shí)時熒光定量RT-PCR法檢測miR-26a-5p及下游分子THAP2轉(zhuǎn)錄水平。流式細(xì)胞技術(shù)分析miR-26a-5p表達(dá)對子宮內(nèi)膜癌細(xì)胞凋亡的影響。結(jié)果:子宮內(nèi)膜癌細(xì)胞Ishikawa與KLE均表達(dá)miR-26a-5p;miR-26a-5p過表達(dá)能增加THAP2的轉(zhuǎn)錄水平,促進(jìn)子宮內(nèi)膜癌細(xì)胞凋亡;miR-26a-5p下調(diào)能抑制THAP2的轉(zhuǎn)錄水平,抑制子宮內(nèi)膜癌細(xì)胞凋亡。結(jié)論:miR-26a-5p可提高THAP2的轉(zhuǎn)錄水平,促進(jìn)子宮內(nèi)膜癌細(xì)胞凋亡,明確這種調(diào)控機(jī)制可能為子宮內(nèi)膜癌預(yù)防診斷和治療帶來新的契機(jī)。
[Abstract]:Objective: to study the effect of miR-26a-5p targeted THAP2 on apoptosis of endometrial carcinoma cells. Methods: the expression of miR-26a-5p in endometrial carcinoma cells was detected by real-time fluorescence quantitative RT-PCR. MiR-26a-5p overexpression and interference plasmids were constructed and transfected into endometrial carcinoma cell line Ishikawa and KLE, real-time quantitative RT-PCR to detect the transcription level of miR-26a-5p and its downstream molecule THAP2. The effect of miR-26a-5p expression on apoptosis of endometrial carcinoma cells was analyzed by flow cytometry. Results: the overexpression of miR-26a-5p;miR-26a-5p in endometrial cancer cells both Ishikawa and KLE increased the transcription level of THAP2 and promoted the apoptosis of endometrial cancer cells. Down-regulation of miR-26a-5p can inhibit the transcription level of THAP2 and inhibit the apoptosis of endometrial cancer cells. Conclusion: miR-26a-5p can improve the transcription level of THAP2 and promote the apoptosis of endometrial cancer cells, which may bring a new opportunity for the prevention, diagnosis and treatment of endometrial carcinoma.
【作者單位】: 上海交通大學(xué)附屬第一人民醫(yī)院;同濟(jì)大學(xué)附屬第一婦嬰保健院;
【基金】:國家自然科學(xué)基金青年項(xiàng)目(No:81001154/H1621)
【分類號】:R737.33
本文編號:2411231
[Abstract]:Objective: to study the effect of miR-26a-5p targeted THAP2 on apoptosis of endometrial carcinoma cells. Methods: the expression of miR-26a-5p in endometrial carcinoma cells was detected by real-time fluorescence quantitative RT-PCR. MiR-26a-5p overexpression and interference plasmids were constructed and transfected into endometrial carcinoma cell line Ishikawa and KLE, real-time quantitative RT-PCR to detect the transcription level of miR-26a-5p and its downstream molecule THAP2. The effect of miR-26a-5p expression on apoptosis of endometrial carcinoma cells was analyzed by flow cytometry. Results: the overexpression of miR-26a-5p;miR-26a-5p in endometrial cancer cells both Ishikawa and KLE increased the transcription level of THAP2 and promoted the apoptosis of endometrial cancer cells. Down-regulation of miR-26a-5p can inhibit the transcription level of THAP2 and inhibit the apoptosis of endometrial cancer cells. Conclusion: miR-26a-5p can improve the transcription level of THAP2 and promote the apoptosis of endometrial cancer cells, which may bring a new opportunity for the prevention, diagnosis and treatment of endometrial carcinoma.
【作者單位】: 上海交通大學(xué)附屬第一人民醫(yī)院;同濟(jì)大學(xué)附屬第一婦嬰保健院;
【基金】:國家自然科學(xué)基金青年項(xiàng)目(No:81001154/H1621)
【分類號】:R737.33
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