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首页> 外文期刊>Journal of Cellular Physiology >MicroRNA‐16 functions as a tumor‐suppressor gene in oral squamous cell carcinoma by targeting AKT3 and BCL2L2
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MicroRNA‐16 functions as a tumor‐suppressor gene in oral squamous cell carcinoma by targeting AKT3 and BCL2L2

机译：微rna量16函数作为一个肿瘤抑制基因在针对AKT3口腔鳞状细胞癌和BCL2L2

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摘要

Aberrant expressions of microRNAs have been reported to be strongly associated with the progression and prognosis of various tumors, including oral squamous cell carcinoma (OSCC). Recent studies on miRNA expression profiling have suggested that microRNA‐16 (miR‐16) may be dysregulated in OSCC. However, the tumorigenic roles and mechanisms of miR‐16 in OSCC are still largely unknown. In this study, we demonstrated that miR‐16 was specifically downregulated in both OSCC patients and cancer cell lines. In addition, functional roles of miR‐16 in vitro suggested that the miR‐16 mimic inhibited cell proliferation and induced apoptosis, whereas miR‐16 inhibitor displayed the opposite effects. Luciferase reporter assay and correlation analysis showed that AKT3 and BCL2L2 were directly targeted by miR‐16 and were inversely expressed with miR‐16 in OSCC. Moreover, restoration of AKT3 and BCL2L2 expression could partially reverse the cell proliferation inhibition and apoptosis induction caused by miR‐16. In xenograft nude mice, miR‐16 mimics decreased the expression of AKT3 and BCL2L2 and reduced the tumors volumes and weights, whereas the miR‐16 inhibitor exhibited adverse effects in the derived xenografts. In conclusion, the findings suggested that miR‐16 functions as a tumor suppressor miRNA to inhibit cell proliferation and induce apoptosis in OSCC through decreasing the oncogenes AKT3 and BCL2L2 and that miR‐16 could be a potential therapeutic target for OSCC.
机译：异常的microrna的表达据报道强烈相关各种肿瘤的进展及预后,包括口腔鳞状细胞癌(OSCC)。最近的研究在microrna的表达分析建议微16(米尔16)应承担的可能在OSCC特异表达。角色和米尔16在OSCC仍应承担的机制很大程度上是未知的。,米尔16是专门表达下调OSCC患者和癌症细胞系。此外,米尔16体外应承担的功能角色建议米尔16模仿抑制细胞增殖和诱导细胞凋亡,而米尔16抑制剂显示了相反的效果。荧光素酶报告实验和相关性分析表明,AKT3和BCL2L2直接目标,米尔16和反向表达与米尔在OSCC 16。恢复AKT3和BCL2L2表达部分逆转细胞增殖抑制和细胞凋亡诱导所致米尔16。减少AKT3 BCL2L2和的表达减少肿瘤体积和重量,而米尔检测16抑制剂表现出负面影响派生的异种移植。研究结果表明,米尔16功能肿瘤抑制microrna的抑制细胞在OSCC增殖和诱导细胞凋亡通过减少致癌基因AKT3 BCL2L2地理,米尔16可能是一个潜在的治疗OSCC的目标。

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