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微小RNA-503通过调控程序性细胞死亡蛋白4促进结肠癌细胞的迁移和侵袭。

MiR-503 promotes the migration and invasion of colorectal cancer cells by regulating PDCD4.

作者信息

Li Lihua, Zhang Xiaolian, Yi Zengxing, Liang Xiaofang, Yin Weihua, Li Shaoyuan

机构信息

Department of Oncology, People's Hospital of Yichun, Jiangxi Province, China.

出版信息

J BUON. 2018 May-Jun;23(3):579-586.

Abstract

PURPOSE

MicroRNAs are expressed abnormally in colorectal cancer (CRC) and could participate in its development. In this study we aimed to explore the molecular mechanisms of miR-503 in the genesis of CRC.

METHODS

The relative expression of miR-503 and programmed cell death 4 (PDCD4) tumor suppressor in CRC tissues and cell lines were detected by qRT-PCR and Western blot. Cell migration and cell invasion were assessed by transwell assay. Moreover, the confirmation of the direct target of miR-503 in CRC was performed by luciferase reporter assay.

RESULTS

The expression of miR-503 was increased remarkably in CRC, while PDCD4 decreased. Moreover, PDCD4 was verified as a specific target of miR-503 in CRC and it could reverse the effect of miR-503 on CRC cells. Furthermore, the abnormal expression of miR-503 played an important role in regulating of the development of CRC cells. In addition, PDCD4 protein expression and miR-503 mRNA expression were negatively correlated in CRC tissues.

CONCLUSION

The inhibitory effect of miR-503 in CRC was realized by the upregulation of PDCD4, suggesting that miR-503/PDCD4 axis might play a critical role in CRC and could possibly be a therapeutic target.

摘要

目的

微小RNA在结直肠癌(CRC)中异常表达,并可能参与其发展。在本研究中,我们旨在探讨miR - 503在CRC发生中的分子机制。

方法

采用qRT - PCR和蛋白质免疫印迹法检测CRC组织和细胞系中miR - 503和程序性细胞死亡4(PDCD4)肿瘤抑制因子的相对表达。通过Transwell实验评估细胞迁移和侵袭能力。此外,通过荧光素酶报告基因实验验证miR - 503在CRC中的直接靶点。

结果

miR - 503在CRC中表达显著增加,而PDCD4表达降低。此外,PDCD4被证实为CRC中miR - 503的特异性靶点,并且它可以逆转miR - 503对CRC细胞的影响。此外,miR - 503的异常表达在调节CRC细胞发展中起重要作用。另外,在CRC组织中,PDCD4蛋白表达与miR - 503 mRNA表达呈负相关。

结论

miR - 503对CRC的抑制作用是通过上调PDCD4实现的,提示miR - 503/PDCD4轴可能在CRC中起关键作用,并且可能成为一个治疗靶点。

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