Department of Otolaryngology, The 1st Affiliated Hospital of Henan University of Science and Technology, Henan, China.
Eur Rev Med Pharmacol Sci. 2018 Sep;22(17):5569-5575. doi: 10.26355/eurrev_201809_15820.
To explore whether microRNA-138 could regulate the incidence and progression of laryngeal carcinoma through modulating proliferation and apoptosis of laryngeal carcinoma cells via MAPK6.
MicroRNA-138 expression in laryngeal carcinoma tissues and paracancerous tissues were detected by qRT-PCR (Quantitative Real-Time Polymerase Chain Reaction). The regulatory effects of microRNA-138 on proliferation and apoptosis of laryngeal carcinoma cells were detected by colony formation assay and flow cytometry, respectively. Target gene of microRNA-138 was predicted by online software and verified by luciferase reporter gene assay. Corresponding plasmids of microRNA-138 and the target gene were constructed. Rescue experiments were conducted to explore the regulatory effect of microRNA-138 on the target gene.
MicroRNA-138 was downregulated in laryngeal carcinoma tissues than that of paracancerous tissues. MicroRNA-138 knockdown resulted in increased proliferation and decreased apoptosis of laryngeal carcinoma cells. MAPK6 was predicted as the target gene of microRNA-138. Luciferase reporter gene assay further verified that MAPK6 could directly bind to microRNA-138. Both mRNA and protein levels of MAPK6 were downregulated after microRNA-13 overexpression in laryngeal carcinoma cells. Rescue experiment results indicated that increased proliferation and decreased apoptosis of laryngeal carcinoma cells resulted from microRNA-13 knockdown were partially reversed by MAPK6 overexpression.
MicroRNA-138 is downregulated in laryngeal carcinoma patients. MicroRNA-138 knockdown promotes proliferation and inhibits apoptosis of laryngeal carcinoma cells via inhibiting MAPK6 expression.
通过调节 MAPK6 探讨微小 RNA-138 是否可以调控喉癌的发生和发展，从而影响喉癌细胞的增殖和凋亡。
采用 qRT-PCR 检测喉癌组织和癌旁组织中微小 RNA-138 的表达。通过集落形成实验和流式细胞术分别检测微小 RNA-138 对喉癌细胞增殖和凋亡的调控作用。通过在线软件预测微小 RNA-138 的靶基因，并通过荧光素酶报告基因实验进行验证。构建微小 RNA-138 和靶基因的相应质粒。进行挽救实验，以探讨微小 RNA-138 对靶基因的调控作用。
微小 RNA-138 在喉癌组织中的表达低于癌旁组织。微小 RNA-138 敲低导致喉癌细胞增殖增加，凋亡减少。MAPK6 被预测为微小 RNA-138 的靶基因。荧光素酶报告基因实验进一步验证了 MAPK6 可以直接与微小 RNA-138 结合。微小 RNA-138 在喉癌细胞中过表达后，MAPK6 的 mRNA 和蛋白水平均下调。挽救实验结果表明，微小 RNA-13 敲低导致的喉癌细胞增殖增加和凋亡减少部分被 MAPK6 过表达逆转。
微小 RNA-138 在喉癌患者中下调。微小 RNA-138 敲低通过抑制 MAPK6 的表达促进喉癌细胞的增殖并抑制其凋亡。
