ESCO2敲低抑制人胃癌細(xì)胞增殖，誘導(dǎo)細(xì)胞凋亡

2018年1月，蘭州大學(xué)生命科學(xué)學(xué)院細(xì)胞生物學(xué)研究所；蘭州大學(xué)基礎(chǔ)醫(yī)學(xué)院醫(yī)學(xué)生理與心理研究所；蘭州大學(xué)**醫(yī)院普外科；蘭州大學(xué)第二醫(yī)院；甘肅省消化道腫瘤重點(diǎn)實(shí)驗(yàn)室(Institute of Cell Biology, School of Life Sciences, Lanzhou University, 222 Tian-Shui South Road, Lanzhou 730000, Gansu, China；Institute of Medical Physiology and Psychology, School of Basic Medical Sciences, Lanzhou University, 199 Dong-Gang West Road, Lanzhou 730000, Gansu,China；Department of General Surgery, The First Hospital of Lanzhou University, 1 Dong-Gang West Road, Lanzhou 730000, Gansu, China；Second Hospital of Lanzhou University, 82 Cui-Yin Door, Lanzhou 730030, Gansu,   China；Key Laboratory of Digestive Tumor of Gansu Province, 82 Cui-Yin Door, Lanzhou 730030, Gansu, China) Yumin Li老師研究團(tuán)隊(duì)在《Biochemical and Biophysical Research Communications》上發(fā)表論文：

“ESCO2 knockdown inhibits cell proliferation and induces apoptosis in human gastric cancer cells”

“ESCO2敲低抑制人胃癌細(xì)胞增殖，誘導(dǎo)細(xì)胞凋亡”

Abstract：

Establishment of cohesion 1 homolog 2 (ESCO2), an essential gene for cohesion regulation and genomic stability, has not been studied in human gastric cancer (GC). We found that ESCO2 knockdown in human GC cell lines dramatically inhibited cell proliferation and induced cell apoptosis in vitro and suppressed tumor xenograft development in vivo. Furthermore, adenosine monophosphate-activated protein kinase (AMPK) was activated following the suppression of its downstream targets, including mammalian target of rapamycin (mTOR) and p70 ribosomal S6 kinase 1 (p70S6K1), and this result was consistent with p53 activation. Significantly, co-immunoprecipitation (Co-IP) analyses indicated that ESCO2 can interact with p53 in GC cells. Taken together, our data demonstrate that ESCO2 is essential for the development of GC and might be a potential therapeutic target for treating GC.

摘要：

內(nèi)聚力1同源物2 (ESCO2)是調(diào)控內(nèi)聚力和基因組穩(wěn)定性的重要基因，目前尚未在人胃癌(GC)中進(jìn)行研究。科研人員發(fā)現(xiàn)ESCO2在體外顯著抑制人胃癌細(xì)胞系細(xì)胞增殖和誘導(dǎo)細(xì)胞凋亡，并在體內(nèi)抑制腫瘤異種移植物的發(fā)育。此外，腺苷單磷酸活化蛋白激酶(AMPK)在抑制其下游靶點(diǎn)后被激活，包括哺乳動(dòng)物雷帕霉素靶點(diǎn)(mTOR)和p70核糖體S6激酶1 (p70S6K1)，這一結(jié)果與p53的激活一致。值得注意的是，共免疫沉淀(Co-IP)分析表明，ESCO2可以與GC細(xì)胞中的p53相互作用。綜上所述，科研人員的數(shù)據(jù)表明，ESCO2對(duì)胃癌的發(fā)展至關(guān)重要，可能是治療胃癌的潛在治療靶點(diǎn)。

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