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首页> 外文期刊>Digestive Diseases and Sciences >Knockdown of RON inhibits AP-1 activity and induces apoptosis and cell cycle arrest through the modulation of Akt/FoxO signaling in human colorectal cancer cells
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Knockdown of RON inhibits AP-1 activity and induces apoptosis and cell cycle arrest through the modulation of Akt/FoxO signaling in human colorectal cancer cells

机译：RON的抑制通过调节人类结直肠癌细胞中的Akt / FoxO信号传导抑制AP-1活性并诱导凋亡和细胞周期停滞

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Background/Aims: Altered Recepteur d'Origine nantais (RON) expression transduces signals inducting invasive growth phenotype that includes cell proliferation, migration, matrix invasion, and protection of apoptosis in human cancer cells. The aims of the current study were to evaluate whether RON affects tumor cell behavior and cellular signaling pathways including activator protein-1 (AP-1) and Akt/forkhead box O (FoxO) in human colorectal cancer cells. Methods: To study the biological role of RON on tumor cell behavior and cellular signaling pathways in human colorectal cancer, we used small interfering RNA (siRNA) to knockdown RON gene expression in human colorectal cancer cell line, DKO-1. Results: Knockdown of RON diminished migration, invasion, and proliferation of human colorectal cancer cells. Knockdown of RON decreased AP-1 transcriptional activity and expression of AP-1 target genes. Knockdown of RON activated cleaved caspase-3, -7, -9, and PARP, and down-regulated the expression of Mcl-1, survivin and XIAP, leading to induction of apoptosis. Knockdown of RON induced cell cycle arrest in the G2/M phase of cancer cells by an increase of p27 and a decrease of cyclin D3. Knockdown of RON inhibited the phosphorylation of Akt/FoxO signaling proteins such as Ser473 and Thr308 of Akt and FoxO1/3a. Conclusions: These results indicate that knockdown of RON inhibits AP-1 activity and induces apoptosis and cell cycle arrest through the modulation of Akt/FoxO signaling in human colorectal cancer cells.
机译：背景/目的：改变的原始受体南泰（RON）表达转导诱导侵入性生长表型的信号，包括细胞增殖，迁移，基质侵袭和对人类癌细胞凋亡的保护。本研究的目的是评估RON是否会影响人大肠癌细胞中的肿瘤细胞行为和细胞信号通路，包括激活蛋白1（AP-1）和Akt /叉头盒O（FoxO）。方法：为了研究RON对人大肠癌肿瘤细胞行为和细胞信号通路的生物学作用，我们使用小干扰RNA（siRNA）敲低人大肠癌细胞系DKO-1中RON基因的表达。结果：敲低RON减少了人类结直肠癌细胞的迁移，侵袭和增殖。敲低RON降低AP-1转录活性和AP-1靶基因的表达。敲低RON激活裂解caspase-3，-7，-9和PARP，并下调Mcl-1，survivin和XIAP的表达，从而诱导凋亡。通过p27的增加和cyclin D3的减少来敲除RON诱导的癌细胞G2 / M期细胞周期停滞。 RON的敲低抑制了Akt / FoxO信号蛋白如Akt和FoxO1 / 3a的Ser473和Thr308的磷酸化。结论：这些结果表明，敲低RON可以通过调节人结肠直肠癌细胞中的Akt / FoxO信号传导来抑制AP-1活性并诱导凋亡和细胞周期停滞。

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