Department of Clinical Laboratory, The First Affiliated Hospital of Xiamen University, Fujian Medical University, Xiamen, Fujian 361003, P.R. China.
Department of Anesthesiology, The First Affiliated Hospital of Xiamen University, Fujian Medical University, Xiamen, Fujian 361003, P.R. China.
Mol Med Rep. 2017 Nov;16(5):6506-6511. doi: 10.3892/mmr.2017.7440. Epub 2017 Sep 8.
MicroRNA (miRNA/miR), a type of non‑coding RNA molecule, is able to inhibit the expression of target genes at multiple stagess. There are 800‑1,000 known miRNAs in the human genome, which serve important roles in cell proliferation, differentiation, apoptosis and migration. Previous studies have demonstrated that the expression of miR‑21 is upregulated in numerous types of malignant tumor, and that miR‑21 participates in the occurrence and development of tumors via complex regulatory mechanisms. The present study aimed to investigate the association between miR‑21 expression, cell viability and apoptosis in a lung cancer cell line, and to elucidate the potential mechanisms. miR‑21 or small interfering RNA against miR‑21 were transfected into A549 non‑small cell lung cancer cells. The mRNA expression of miR‑21 was confirmed. Cell viability and apoptosis were examined using MTT and flow cytometric assays, respectively. The expression of certain apoptosis‑associated proteins was detected by western blotting. The results of the present study demonstrated that miR‑21 was able to increase the proliferation of A549 cells by inhibiting cellular apoptosis. miR‑21 inhibited apoptosis by modulating the activation of the phosphatidylinositol 3‑kinase/Rac‑α serine/threonine protein kinase (Akt) pathway in A549 cells. Correspondingly, inhibition of Akt decreased the apoptosis of A549 cells in miR‑21 siRNA‑treated cells. Therefore, the results of the present study demonstrated that miR‑21 increased cell viability by inhibiting apoptosis, through regulation of Akt activation. The present study demonstrated that miR‑21 may be involved in the progression of lung cancer and may be a novel therapeutic target for the disease.
微小 RNA（miRNA/miR）是一种非编码 RNA 分子，能够在多个阶段抑制靶基因的表达。人类基因组中约有 800-1000 种已知的 miRNA，它们在细胞增殖、分化、凋亡和迁移中发挥重要作用。先前的研究表明，miR-21 在多种恶性肿瘤中表达上调，并且 miR-21 通过复杂的调控机制参与肿瘤的发生和发展。本研究旨在探讨 miR-21 表达、肺癌细胞活力和细胞凋亡之间的关系，并阐明其潜在机制。将 miR-21 或针对 miR-21 的小干扰 RNA 转染至 A549 非小细胞肺癌细胞中。证实 miR-21 的 mRNA 表达。分别采用 MTT 和流式细胞术检测细胞活力和细胞凋亡。采用 Western blot 检测某些凋亡相关蛋白的表达。本研究结果表明，miR-21 通过抑制细胞凋亡增加 A549 细胞的增殖。miR-21 通过调节 A549 细胞中磷脂酰肌醇 3-激酶/Rac-α丝氨酸/苏氨酸蛋白激酶（Akt）通路的激活来抑制细胞凋亡。相应地，在 miR-21 siRNA 处理的细胞中抑制 Akt 降低了 A549 细胞的凋亡。因此，本研究结果表明，miR-21 通过调节 Akt 激活抑制细胞凋亡，从而增加细胞活力。本研究表明，miR-21 可能参与肺癌的进展，并且可能是该疾病的一种新的治疗靶点。
