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首页> 外文期刊>Journal of cellular physiology. >Silencing of RHEB inhibits cell proliferation and promotes apoptosis in colorectal cancer cells via inhibition of the mTOR signaling pathway
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Silencing of RHEB inhibits cell proliferation and promotes apoptosis in colorectal cancer cells via inhibition of the mTOR signaling pathway

机译：沉默的RHEB抑制细胞增殖通过促进细胞凋亡在结直肠癌细胞抑制mTOR的信号通路

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摘要

Colorectal cancer (CRC) is commonly known as one of the most prominent reasons for cancer-related death in China. Ras homolog enriched in brain (RHEB) and the mammalian target activity of rapamycin (mTOR) signaling pathway were found correlated with CRC, but their specific interaction in CRC was still to be investigated. Therefore, we explored whether RHEB gene silencing affected the cell proliferation, differentiation, and apoptosis by directly targeting the mTOR signaling pathway in cells previously harvested from CRC patients. A microarray analysis was subsequently conducted to investigate the relationship between RHEB and mTOR. Eighty-three adjacent normal tissues and CRC tissues were selected. Immunohistochemistry was carried out to detect the positive expression rates of RHEB and Ki-67 in the CRC tissues. Cells were then transfected with different siRNAs to investigate the potential effects RHEB would have on CRC progression. The expressions of RHEB, 4EBP1, ribosomal protein S6 kinase (p70S6K), proliferating cell nuclear antigen (PCNA), B cell lymphoma 2 (bcl-2), and bcl-2-associated X protein (bax) were determined and then the cell cycle, cell proliferation, and apoptotic rate were also measured. We identified RHEB and mTOR as upregulated genes in CRC. Cells treated with RHEB silencing showed a decreased extent of mTOR, p70S6K, 4EBP1 phosphorylation and expression of RHEB, Ki-67, mTOR, p70S6K, 4EBP1, bcl-2, and PCNA as well as decreased activity of cell proliferation and differentiation; although, the expression of bax was evidently higher. Collectively, our data propose the idea that RHEB gene silencing might repress cell proliferation and differentiation while accelerating apoptosis via inactivating the mTOR signaling pathway.
机译：结直肠癌(CRC)通常被称为一个最著名的癌症相关的理由死在中国。(RHEB)和哺乳动物的目标的活动雷帕霉素(mTOR)信号通路被发现与CRC,但是他们的具体互动CRC仍在调查。因此,我们探讨是否RHEB基因沉默影响细胞增殖,直接分化,细胞凋亡针对mTOR信号通路在细胞以前是从CRC患者。微阵列分析随后进行调查RHEB和之间的关系mTOR。CRC组织选择。积极的表达进行检测利率CRC RHEB和ki - 67的组织。然后转染不同siRNAs调查RHEB会潜在影响CRC进展。4 ebp1,核糖体蛋白S6激酶(p70S6K),增殖细胞核抗原),B细胞淋巴瘤2 (bcl - 2), bcl-2-associated X蛋白(伯灵顿)测定细胞周期、细胞增殖和凋亡率也被测量。CRC的调节基因。RHEB沉默显示减少mTOR的程度,p70S6K 4 ebp1磷酸化和表达RHEB Ki-67, mTOR, 4EBP1, bcl-2 p70S6K和PCNA以及减少活动的细胞增殖和分化;伯灵顿的表情显然更高。总的来说,我们的数据提出RHEB基因沉默可能抑制细胞增殖在加速细胞凋亡和分化通过灭活mTOR信号通路。

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