miR-30a suppresses lung cancer progression by targeting SIRT1
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Yaowu Guan1, Zhongming Rao1 and Cheng Chen2
1Department of Thoracic Surgery, Zhumadian Central Hospital, Zhumadian, Henan 463000, China
2Department of Radiotherapy, Nanjing Medical University Affiliated Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu 210009, China
Yaowu Guan, email: [email protected]
Cheng Chen, email: [email protected]
Keywords: miR-30a; SIRT1; proliferation; apoptosis; invasion
Abbreviations: SIRT1: silent information regulator 1; miRNA: microRNA
Received: September 15, 2017 Accepted: December 04, 2017 Published: December 21, 2017
The class III histone deacetylase silent information regulator 1 (SIRT1) is frequently overexpressed in a variety of tumors, including lung cancer; however, its regulatory mechanisms are largely unknown. In this study, we found that an inconsistent trend between SIRT1 protein and mRNA levels in human lung cancer tissues, suggesting that a post-transcriptional mechanism may involved in SIRT1 regulation. Because microRNAs are important post-transcriptional regulators of gene expression, candidate miRNAs that could potentially bind SIRT1 were gained through bioinformatics analyses. We further experimentally validated SIRT1 as the direct target of miR-30a by evaluating SIRT1 expression in lung cancer cells after the overexpression or knockdown of miR-30a and by luciferase assay. Moreover, we showed that miR-30a inhibited proliferation, invasion and promoted apoptosis of lung cancer cells by inhibiting SIRT1 in vitro and in vivo. Taken together, this study identified a new regulatory axis in which miR-30a and SIRT1 regulate the proliferation, invasion and apoptosis of lung cancer cells and lung tumorigenesis.
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