Li Xiangyong, Liu Fumei, Lin Bihua, Luo Haiqing, Liu Meilian, Wu Jinhua, Li Caihong, Li Ronggang, Zhang Xin, Zhou Keyuan, Ren Dong
Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Key Laboratory of Medical Bioactive Molecular Research for Department of Education of Guangdong Province, Guangdong Medical University, Dongguan, Guangdong 523808, P.R. China.
Int J Oncol. 2017 Apr;50(4):1097-1108. doi: 10.3892/ijo.2017.3909. Epub 2017 Mar 10.
Cancer cells are characterized by a pathological manifestation of uncontrolled proliferation, which results in tumor formation. Therefore, it is necessary to improve understanding of the underlying mechanism of cell cycle control. Here, we report that miR‑150 is downregulated in nasopharyngeal carcinoma tissues and cells. Upregulation of miR‑150 suppresses nasopharyngeal carcinoma (NPC) cell proliferation and induces G1/S arrest in vitro, and inhibits tumorigenesis in vivo. Conversely, silencing miR‑150 yields the opposite effect. Our results further demonstrate that miR‑150 retards nasopharyngeal carcinoma cell proliferation and G1/S transition via targeting multiple cell cycle-related genes, including CCND1, CCND2, CDK2 and CCNE2. Therefore, our results uncover a novel mechanistic understanding of miR‑150-mediated tumor suppression in NPC, which will facilitate the development of effective cancer therapies against nasopharyngeal carcinoma.
癌细胞的特征是不受控制的增殖这一病理表现，其导致肿瘤形成。因此，有必要增进对细胞周期调控潜在机制的理解。在此，我们报告miR-150在鼻咽癌组织和细胞中表达下调。miR-150的上调抑制鼻咽癌（NPC）细胞增殖并在体外诱导G1/S期阻滞，且在体内抑制肿瘤发生。相反，沉默miR-150则产生相反的效果。我们的结果进一步证明，miR-150通过靶向多个细胞周期相关基因（包括CCND1、CCND2、CDK2和CCNE2）来延缓鼻咽癌细胞增殖和G1/S期转换。因此，我们的结果揭示了对miR-150介导的鼻咽癌肿瘤抑制的新机制理解，这将有助于开发针对鼻咽癌的有效癌症治疗方法。
