Gastric cancer (GC) accounts for a main cause of cancer-related deaths. This study sought for molecular mechanism of miR-490-5p/DTL axis in affecting GC progression, thus bringing new hope for treatment of GC. Expression data of differentially expressed miRNAs and mRNAs in GC tissue from TCGA database were analyzed. MiR-490-5p and DTL mRNA expression levels in GC were evaluated with qRT-PCR. Cell viability was confirmed with CCK-8 method. Cell cycle distribution and apoptosis were analyzed with flow cytometry. Cell migratory and invasive potential was proved with Transwell assay. The targeted relationship between DTL and miR-490-5p was analyzed with dual-luciferase assay. The results indicated a decreased miR-490-5p level in GC cells. MiR-490-5p upregulation hampered proliferation, migration, invasion and promote cell apoptosis. DTL was the target of and inversely associated with miR-490-5p, and it could remarkably induce the carcinogenesis of GC. MiR-490-5p mediated GC cell progression by DTL repression. In conclusion, miR-490-5p and DTL may be valuable in diagnosis and treatment for GC.

中文翻译：

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MiR-490-5p 通过 DTL 抑制抑制胃癌的进展

胃癌 (GC) 是癌症相关死亡的主要原因。本研究探索miR-490-5p/DTL轴影响GC进展的分子机制，为GC治疗带来新希望。分析了来自TCGA数据库的GC组织中差异表达的miRNA和mRNA的表达数据。用 qRT-PCR 评估 GC 中 MiR-490-5p 和 DTL mRNA 的表达水平。用CCK-8方法确认细胞活力。用流式细胞术分析细胞周期分布和细胞凋亡。Transwell 试验证明了细胞迁移和侵袭的潜力。用双荧光素酶测定法分析了DTL与miR-490-5p之间的靶向关系。结果表明GC细胞中miR-490-5p水平降低。MiR-490-5p 上调阻碍增殖、迁移、侵袭并促进细胞凋亡。DTL是miR-490-5p的靶点并与miR-490-5p呈负相关，可显着诱导GC的癌变。MiR-490-5p 通过 DTL 抑制介导 GC 细胞进展。总之，miR-490-5p 和 DTL 可能对 GC 的诊断和治疗有价值。