Abstract

BackgroundEmerging evidence reveals that microRNAs (miRNAs) play a crucial role in tumor progression, but the underlying mechanism of microRNAs in lung squamous cell cancer (LSCC) remains unclear.MethodWestern-blotting and quantitative real-time PCR (q-PCR) were carried out to detect mRNA and protein expression. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8), colony-forming assay or sphere-forming assay, respectively.ResultsMiR-214-3p was markedly de-regulated in LSCC tissues and was inversely related to the level of Yes-associated protein1 (YAP1), which is the core transcription regulator of the Hippo signaling pathway. Kaplan–Meier survival curves illustrated that patients with high miR-214-3p expression demonstrated more favorable clinical outcomes. MiR-214-3p overexpression (OE) repressed proliferation and cancer stem-like cells (CSCs) properties in vitro and in vivo xenograft mouse model. Mechanistically, luciferase activity assay revealed that miR-214-3p directly targets YAP1 by specifically binding on the 3′ UTR of YAP1.ConclusionMiR-214-3p plays a pivotal role in CSCs properties by targeting YAP1, which provides a potential treatment strategy for LSCC patients.

Highlights

  • Emerging evidence reveals that microRNAs play a crucial role in tumor progression, but the underlying mechanism of microRNAs in lung squamous cell cancer (LSCC) remains unclear

  • We reported that miR-214-3p inhibited cancer stem cells (CSCs) capacity by targeting Yes-associated protein1 (YAP1) in LSCC

  • MiR‐214‐3p is downregulated in LSCC and is significantly associated with better clinical prognosis While YAP1 is elevated, the miR-214-3p is downregulated in tumor species compared to the matched normal bronchial epithelium using quantitative real-time PCR (q-PCR) analysis [19, 20]

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Summary

Introduction

Emerging evidence reveals that microRNAs (miRNAs) play a crucial role in tumor progression, but the underlying mechanism of microRNAs in lung squamous cell cancer (LSCC) remains unclear. Compared with AC, the mainstream treatment regimens for lung squamous cell cancer (LSCC) are still platinum-containing chemotherapeutics and immune therapy, and the targeted therapy for MicroRNAs are a cluster of noncoding RNAs that modulate gene expression [2]. Increasing evidence has shown that aberrant miRNA expression participates in diverse pathogenic processes, such as tumor apoptosis and CSC properties [3,4,5,6]. MiR-205 OE remarkably decreases the proliferation of CSCs in human pancreatic cancer [10] while low expression of miR-613 contributed to the

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