Abstract
BackgroundLung adenocarcinoma (LUAD) is a subtype of lung cancer (LC), which is the most common tumor worldwide. Accumulating evidence has elucidated an important role of microRNAs (miRNAs) in mediating the development and progression of several tumors. The purpose of this study was to explore the role and underlying mechanism of miR‐15b in LUAD.MethodsCCK‐8 and Transwell assays were conducted to measure the capacities of cell viability and migration in SPC‐A1 cells. Luciferase assay was utilized to verifymiR‐15b direct binding to BCL2 mRNA 3′‐UTR.ResultsWe determined that miR‐15b was overexpressed in LUAD and miR‐15b overexpression predicted a significantly worse outcome in patients with LUAD. miR‐15b improved LUAD growth in vitro and vivo. miR‐15b enhanced cell migration and epithelial–mesenchymal transition (EMT) in LUAD. miR‐15b promoted cell viability, migration and EMT through inhibiting BCL2 expression by targeting to its mRNA 3′‐UTR. BCL2 reversed functions of miR‐15b on promoting cell proliferation, migration and EMT in SPC‐A1 cells.ConclusionsmiR‐15b promoted cell viability, migration and EMT by targeting BCL2 in LUAD. The newly identified miR‐15b/BCL2 axis provides a novel insight into the pathogenesis of LUAD.
Highlights
Lung cancer (LC) is the leading cause of cancer-related mortality worldwide, with lung adenocarcinoma (LUAD) being the most frequently diagnosed histological subtype.[1,2] Most patients with Lung adenocarcinoma (LUAD) are usually diagnosed at advanced stages and have a poor prognosis.[3,4] It is necessary to define new molecular biomarkers for the early diagnosis of LUAD.MicroRNAs are endogenous non-coding RNAs containing 18–25 nucleotides.[5]
N-cadherin and vimentin expression was decreased by miR-15b inhibitor, while E-cadherin expression was increased by miR-15b inhibitor in APC-A1 cells (Fig 3c), suggesting that miR-15b enhanced the epithelial–mesenchymal transition (EMT) ability in LUAD
Lung adenocarcinoma is a subtype of NSCLC that accounts for 40% of total lung cancer (LC).[28]
Summary
MicroRNAs (miRNAs) are endogenous non-coding RNAs containing 18–25 nucleotides.[5] MiRNAs mediate the repression of translation to regulate the expression of target genes at post-transcriptional levels.[6,7] In this way, miRNAs may play important roles in several processes that include adhesion, differentiation, cell death and metastasis.[8,9] MiR15b was upregulated and acted as an oncogene in multiple diseases, including hepatocellular carcinoma, ovarian cancer and chronic neuropathic pain.[10,11,12] MiR-15b facilitated tumorigenicity by enhancing growth and invasiveness, and predicted tumor recurrence in prostate cancer.[13] MiR-15b may act as an independent risk factor that has been associated with a poor outcome for cervical carcinoma patients.[14] miR-15b acted as a tumor suppressor to inhibit cell proliferation of osteosarcoma.[15] The expression and the regulatory mechanism is still unclear in LUAD. MiR-15b promoted cell viability, migration and EMT through inhibiting BCL2 expression by targeting to its mRNA 30-UTR. BCL2 reversed functions of miR-15b on promoting cell proliferation, migration and EMT in SPC-A1 cells. Conclusions: miR-15b promoted cell viability, migration and EMT by targeting BCL2 in LUAD. The newly identified miR-15b/BCL2 axis provides a novel insight into the pathogenesis of LUAD
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