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首页> 外文期刊>Cellular Physiology and Biochemistry >Gastric Adenocarcinoma Predictive Long Intergenic Non-Coding RNA Promotes Tumor Occurrence and Progression in Non-Small Cell Lung Cancer via Regulation of the miR-661/eEF2K Signaling Pathway
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Gastric Adenocarcinoma Predictive Long Intergenic Non-Coding RNA Promotes Tumor Occurrence and Progression in Non-Small Cell Lung Cancer via Regulation of the miR-661/eEF2K Signaling Pathway

机译：胃腺癌预测性长基因间非编码RNA通过调节miR-661 / eEF2K信号通路促进非小细胞肺癌的肿瘤发生和发展。

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Background/Aims Long non-coding RNAs (lncRNAs) play vital roles in carcinogenesis as oncogenes or tumor suppressor genes. This study explored the biological function of lncRNA gastric adenocarcinoma predictive long intergenic non-coding RNA (GAPLINC) in human non-small cell lung cancer (NSCLC). Methods GAPLINC expression in NSCLC specimens and cell lines was detected by qRT-PCR and Western blot. The effect of GAPLINC on cell proliferation was investigated using CCK8-assay, colony formation assay, and xenograft model. The effects of GAPLINC on apoptosis and cell cycle were determined using flow cytometry. The mechanism of GAPLINC involved in NSCLC was explored using Western blot, luciferase reporter assay, and RNA fluorescence in situ hybridization. Results We found that GAPLINC expression was up-regulated in NSCLC tissues and cell lines. Overexpression of GAPLINC was associated with poor prognosis in patients with NSCLC. Silencing of GAPLINC significantly inhibited cell proliferation, promoted apoptosis, and induced cell cycle arrest in the G0/G1 phase. Results from xenograft transplantation showed that GAPLINC silencing inhibited the tumor growth in vivo. Interestingly, GAPLINC silencing decreased the expression of eukaryotic elongation factor-2 kinase (eEF2K) protein both in vivo and in vitro. Bioinformatic analysis and luciferase reporter confirmed that miR-661 targeted GAPLINC and eEF2K 3’-UTR and was negatively correlated with the expression of GAPLINC and eEF2K. Conclusion Our findings indicate that GAPLINC promotes NSCLC tumorigenesis by regulating miR-661/eEF2K cascade and provide new insights for the pathogenesis underlying NSCLC and potential targets for therapeutic strategy.
机译：背景/目的长的非编码RNA（lncRNA）在癌发生过程中作为癌基因或抑癌基因发挥着至关重要的作用。这项研究探讨了lncRNA胃腺癌预测长基因间非编码RNA（GAPLINC）在人非小细胞肺癌（NSCLC）中的生物学功能。方法采用qRT-PCR和Western blot检测NSCLC标本和细胞株中GAPLINC的表达。使用CCK8分析，集落形成分析和异种移植模型研究了GAPLINC对细胞增殖的影响。使用流式细胞术确定GAPLINC对细胞凋亡和细胞周期的影响。利用蛋白质印迹，荧光素酶报告基因分析和RNA荧光原位杂交探索了GAPLINC参与NSCLC的机制。结果我们发现GAPLINC在NSCLC组织和细胞系中的表达上调。 GAPLINC的过表达与NSCLC患者的预后不良有关。沉默GAPLINC可以显着抑制细胞增殖，促进细胞凋亡，并诱导细胞周期停滞在G0 / G1期。异种移植的结果表明，GAPLINC沉默可抑制体内肿瘤的生长。有趣的是，GAPLINC沉默在体内和体外均降低了真核延伸因子2激酶（eEF2K）蛋白的表达。生物信息学分析和荧光素酶报告基因证实，miR-661靶向GAPLINC和eEF2K 3'-UTR，与GAPLINC和eEF2K的表达呈负相关。结论我们的发现表明，GAPLINC通过调节miR-661 / eEF2K级联促进NSCLC的肿瘤发生，并为NSCLC的潜在发病机理和治疗策略的潜在靶点提供了新的见解。

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