2019•Biomedicine & PharmacotherapyOpen access

MiR-183-5p is required for non-small cell lung cancer progression by repressing PTEN

Huimin Wang, Zhongliang Ma, Xiaomin Liu, Caiyan Zhang, Yanping Hu, Ding Lei, Pengfei Qi, Ju Wang, Shengdi Lu, Yanli Li

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Abstract

Lung cancer is the leading cause in all cancer deaths. A low survival rate and high recurrence rate of lung cancer make the endeavor to identify new, more effective therapies a primary goal. MicroRNAs (miRNAs) are regarded as regulators of tumorigenesis and it is known that miR-183-5p is significantly upregulated in non-small cell lung cancer (NSCLC), suggesting it has an oncogenic function in lung cancer. In this study, we found that miR-183-5p could promote lung carcinogenesis by directly targeting phosphatase tensin (PTEN). Further experiments indicated that miR-183-5p could suppress p53 and activate AKT signaling through phosphorylation. Moreover, our data indicated that miR-183-5p promoted tumor metastasis and tumor growth in vivo. Collectively, these results showed that miR-183-5p is required for NSCLC development through the suppressing PTEN, and might be a promising target in the diagnosis and treatment of lung cancer in the future.

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What this paper is about

Lung cancer is the leading cause in all cancer deaths. A low survival rate and high recurrence rate of lung cancer make the endeavor to identify new, more effective therapies a primary goal. MicroRNAs (miRNAs) are regarded as regulators of tumorigenesis and it is known that miR-183-5p is significantly upregulated in non-small cell lung cancer (NSCLC), suggesting it has an oncogenic function in lung cancer. In this study, we found that miR-183-5p could promote lung carcinogenesis by directly targeting phosphatase tensin (PTEN). Further experiments indicated that miR-183-5p could suppress p53 and activate AKT signaling through phosphorylation. Moreover, our data indicated that miR-183-5p promoted tumor metastasis and tumor growth in vivo. Collectively, these results showed that miR-183-5p is required for NSCLC development through the suppressing PTEN, and might be a promising target in the diagnosis and treatment of lung cancer in the future.

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Available abstract

Lung cancer is the leading cause in all cancer deaths. A low survival rate and high recurrence rate of lung cancer make the endeavor to identify new, more effective therapies a primary goal. MicroRNAs (miRNAs) are regarded as regulators of tumorigenesis and it is known that miR-183-5p is significantly upregulated in non-small cell lung cancer (NSCLC), suggesting it has an oncogenic function in lung cancer. In this study, we found that miR-183-5p could promote lung carcinogenesis by directly targeting phosphatase tensin (PTEN). Further experiments indicated that miR-183-5p could suppress p53 and activate AKT signaling through phosphorylation. Moreover, our data indicated that miR-183-5p promoted tumor metastasis and tumor growth in vivo. Collectively, these results showed that miR-183-5p is required for NSCLC development through the suppressing PTEN, and might be a promising target in the diagnosis and treatment of lung cancer in the future.

Key concepts: PTEN, Tensin, Lung cancer, Carcinogenesis, Cancer research, Metastasis, microRNA, Protein kinase B

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