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Overexpression of tripartite motif containing 26 inhibits non-small cell lung cancer cell growth by suppressing PI3K/AKT signaling

机译:通过抑制PI3K / AKT信号传导,三方基序的过度表达抑制非小细胞肺癌细胞生长

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It has been reported that tripartite motif containing 26 (TRIM26) is involved in the tumorigenesis of some cancers, but its function in non-small cell lung cancer (NSCLC) is still unclear. In this study, we found that TRIM26 was markedly down-regulated in both of NSCLC tumor tissues and cell lines. Additionally, high expression of TRIM26 in NSCLC patients predicted a positive index for patients' overall survival. What is more, overexpression of TRIM26 significantly suppressed NSCLC cell growth. Our further studies indicated that overexpression of TRIM26 inhibited the phosphorylation of PI3K p85 and AKT. And overexpressed TRIM26 regulated cell cycle-related genes' expression, including downregulating CDK4, Cyclin A, Cyclin D1, Cyclin D3, and Cyclin E, and upregulating p27 expression. Finally, we found that TRIM26 up-regulated PTEN expression by stabilizing PTEN protein in NSCLC cells. Collectively, our present study indicated that TRIM26 was decreased in NSCLC and overexpression of TRIM26 inhibited NSCLC cell growth by suppressing PI3K/AKT pathway, which suggested that TRIM26 could be as a potential target for the treatment of NSCLC in the future.
机译:据报道,含26(TRIM26)三方主题涉及某些癌症的肿瘤,但其在非小细胞肺癌(NSCLC)的功能目前还不清楚。在这项研究中,我们发现,TRIM26显着在这两个NSCLC肿瘤组织和细胞系的下调。另外,在NSCLC患者TRIM26的高表达预测患者的总体生存正折射率。更重要的是,TRIM26的表达显著抑制肺癌细胞的生长。我们进一步的研究表明,TRIM26的表达抑制PI3K P85和AKT的磷酸化。和过表达TRIM26调节细胞周期相关基因的表达,包括下调CDK4,细胞周期蛋白A,细胞周期蛋白D1,细胞周期蛋白D3,细胞周期蛋白和E,和上调p27的表达。最后,我们发现,TRIM26通过在NSCLC细胞稳定PTEN蛋白上调PTEN表达。总的来说,我们目前的研究表明,TRIM26在NSCLC降低,TRIM26的过表达通过抑制PI3K / AKT途径,这表明,TRIM26可作为在以后的治疗非小细胞肺癌的潜在靶标抑制NSCLC细胞生长。

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