Wang Jinchun, Wu Jie, Wang Lei, Min Xuewen, Chen Zhujing
Department of Pharmacy, Jiangsu Health Vocational College, Nanjing, Jiangsu 211800, China.
Department of Outpatient, Jurong People's Hospital, Jurong, Zhenjiang, Jiangsu 212400, China.
J Oncol. 2021 Oct 16;2021:1173869. doi: 10.1155/2021/1173869. eCollection 2021.
Gastric cancer (GC) is the most common gastrointestinal cancer and the main cause of tumor-related death. Exploring markers for early diagnosis and new therapeutic targets is always on the way. In the last 10 years, long noncoding RNAs (lncRNAs) have been widely proved to be involved in the progress of many tumors and are regarded as potential targets for tumor therapy. We found that LINC00152, a newly identified lncRNA, was significantly upregulated in GC tissues and affected clinicopathological characteristics in GC patients. Furthermore, we observed that LINC00152 knockdown can significantly reduce cell proliferation and promote apoptosis in human gastric cancer cells. Further bioinformatic analysis indicated that LINC00152 competitively bound with miR-138 and regulated the expression of miR-138. Moreover, SIRT2 was further proved to be a downstream target of miR-138. Overall, this study elucidates the molecular mechanism of LINC00152 underlying the malignant phenotype of GC cells by mediating miR-138/SIRT2 axis, which provides a new understanding of the role and molecular mechanism of lncRNA in GC and also provides a new way for the treatment of gastric cancer.
胃癌（GC）是最常见的胃肠道癌症，也是肿瘤相关死亡的主要原因。探索早期诊断标志物和新的治疗靶点的工作一直在进行中。在过去十年中，长链非编码RNA（lncRNAs）已被广泛证明参与多种肿瘤的进展，并被视为肿瘤治疗的潜在靶点。我们发现，新鉴定的lncRNA LINC00152在GC组织中显著上调，并影响GC患者的临床病理特征。此外，我们观察到敲低LINC00152可显著降低人胃癌细胞的增殖并促进其凋亡。进一步的生物信息学分析表明，LINC00152与miR-138竞争性结合并调节miR-138的表达。此外，SIRT2被进一步证明是miR-138的下游靶点。总体而言，本研究阐明了LINC00152通过介导miR-138/SIRT2轴影响GC细胞恶性表型的分子机制，这为深入了解lncRNA在GC中的作用和分子机制提供了新的认识，也为胃癌治疗提供了新途径。
