DNA損傷誘導(dǎo)的長(zhǎng)鏈非編碼RNA-UCA1促進(jìn)HeLa細(xì)胞增殖
本文選題:長(zhǎng)鏈非編碼RNA 切入點(diǎn):尿路上皮癌抗原(UCA) 出處:《中國(guó)生物化學(xué)與分子生物學(xué)報(bào)》2015年05期 論文類(lèi)型:期刊論文
【摘要】:尿路上皮癌抗原1(UCA1)是一種長(zhǎng)鏈非編碼RNA,在多種腫瘤內(nèi)高表達(dá).然而,其在宮頸癌細(xì)胞和組織中的表達(dá)報(bào)告頗不一致,且功能尚未確定.本文探索UCA1在宮頸癌He La細(xì)胞中的生物學(xué)功能.實(shí)時(shí)定量PCR(qRT-PCR)結(jié)果顯示,UCA1、p21和p53 mRNA在阿霉素(doxorubicin,DOX)或γ射線照射的He La細(xì)胞中表達(dá)上調(diào);相反,敲減p53表達(dá)則可抑制DOX誘導(dǎo)的UCA1上調(diào).表明DNA損傷誘導(dǎo)的UCA1可能與p53有關(guān).轉(zhuǎn)染結(jié)合CCK8檢測(cè)He La細(xì)胞增殖活力結(jié)果顯示,與對(duì)照比較,過(guò)表達(dá)UCA1促進(jìn)He La細(xì)胞增殖,干擾UCA1表達(dá)則減緩細(xì)胞增殖.此外,流式細(xì)胞術(shù)結(jié)果顯示,過(guò)表達(dá)UCA1導(dǎo)致阿霉素誘導(dǎo)的凋亡率下降;siRNA抑制UCA1表達(dá)后引起細(xì)胞G2/M期比例上升,S期下降,且阿霉素誘導(dǎo)的細(xì)胞凋亡率上升.上述結(jié)果說(shuō)明,DNA損傷誘導(dǎo)的UCA1可促進(jìn)He La細(xì)胞增殖,減少細(xì)胞凋亡.然而,是否DNA損傷誘導(dǎo)的UCA1上調(diào)依賴(lài)p53尚需進(jìn)一步實(shí)驗(yàn)證明.
[Abstract]:Urothelial carcinoma antigen (UCA1) is a long chain noncoding RNAs that are highly expressed in many tumors. However, the reports of UCA1 expression in cervical cancer cells and tissues are quite inconsistent. In this study, we investigated the biological function of UCA1 in cervical cancer He-La cells. The results of real-time quantitative PCRQRT-PCR showed that the expression of UCA1p21 and p53 mRNA was up-regulated in doxorubicindoxindoxindoxindoxindoxindoxindoxindoxindox (doxorubicindoxindoxindoxindoxindox doxindoxindox doxindo@@. Knockout p53 could inhibit the up-regulation of UCA1 induced by DOX, suggesting that the UCA1 induced by DNA damage might be related to p53. The results of transfection combined with CCK8 showed that overexpression of UCA1 could promote the proliferation of He-La cells. In addition, flow cytometry showed that overexpression of UCA1 resulted in a decrease in apoptosis induced by doxorubicin. After inhibiting the expression of UCA1, the ratio of G _ 2 / M phase increased and S phase decreased. These results suggest that UCA1 induced by DNA damage can promote the proliferation of He-La cells and reduce apoptosis. However, whether the up-regulation of UCA1 induced by DNA damage depends on p53 should be further demonstrated.
【作者單位】: 大連大學(xué)附屬中山醫(yī)院;軍事醫(yī)學(xué)科學(xué)院放射與輻射醫(yī)學(xué)研究所;大連大學(xué)生命科學(xué)與技術(shù)學(xué)院;
【基金】:國(guó)家自然科學(xué)基金(No.31270836,No.31470782,No.31370760) 北京市自然科學(xué)基金(No.7101007)資助~~
【分類(lèi)號(hào)】:R737.33
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