Abstract
MicroRNAs (miRNAs) have essential roles in carcinogenesis and tumor progression. Here, we investigated the roles and mechanisms of miR-143 in non-small cell lung cancer (NSCLC). miR-143 was significantly decreased in NSCLC tissues and cell lines. Overexpression of miR-143 suppressed NSCLC cell proliferation, induced apoptosis, and inhibited migration and invasion in vitro. Integrated analysis identified LIM domain kinase 1 (Limk1) as a direct and functional target of miR-143. Overexpression of Limk1 attenuated the tumor suppressive effects of miR-143 in NSCLC cells. Moreover, miR-143 was inversely correlated with Limk1 expression in NSCLC tissues. Together, our results highlight the significance of miR-143 and Limk1 in the development and progression of NSCLC.
Highlights
Non-small cell lung cancer (NSCLC), including adenocarcinoma and squamous cell carcinoma, is the leading cause of cancer deaths worldwide [1]
The results showed that miR-143 expression was significantly down-regulated in non-small cell lung cancer (NSCLC) tissues compared with matched controls (Figure 1A)
Aberrant miRNA expression has been implicated in almost all aspects of tumor biology, including proliferation, apoptosis, migration, and invasion, and they can act as either tumor suppressors or oncogenes
Summary
Non-small cell lung cancer (NSCLC), including adenocarcinoma and squamous cell carcinoma, is the leading cause of cancer deaths worldwide [1]. Despite an increasing number of studies on NSCLC genomics as well as the development of targeted therapies, the overall 5-year survival rate is only 15%. This highlights the need for a better understanding of NSCLC biology to improve the prevention, diagnosis, and treatment of this cancer [2]. MiRNA profiling studies have indicated that miR-143 is decreased in several tumor tissues, including NSCLC [15,16,17]. We demonstrate that decreased miR-143 expression is a characteristic molecular signature in NSCLC and that miR-143 may function as a tumor suppressor by directly targeting LIM domain kinase 1 (Limk1)
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