Abstract
ObjectivesLncRNA nuclear‐enriched abundant transcript 1 (NEAT1) participates in the development and progression of multiple malignancies. However, the molecular mechanism by which NEAT1 contributes to colorectal cancer (CRC) remains unclear.MethodsThe association between lncRNA NEAT1 expression and clinicopathological characteristics and prognosis in patients with CRC was analysed by TCGA RNA‐sequencing data. MTT, colony formation, flow cytometry, transwell assays and a xenograft tumour model were used to assess the functions of NEAT1. Bioinformatics and spearman correlation analysis were used to identify the NEAT1‐specific binding with miRNAs, and luciferase gene report and RIP assays were performed to confirm the interaction between miR‐193a‐3p (miR‐193a) and NEAT1 in CRC cells.ResultsUpregulation of NEAT1 expression was significantly correlated with TNM stage, poor survival and tumour recurrence in patients with CRC, and acted as an independent prognostic factor for tumour recurrence. Knockdown of NEAT1 suppressed cell proliferation, colony formation abilities and invasive potential and induced cell apoptosis, but overexpression of NEAT1 reversed these effects. Furthermore, NEAT1 was confirmed to act as a sponge of miR‐193a, and knockdown of NEAT1 attenuated miR‐193a inhibitor‐induced tumour promoting effects and L17RD expression in CRC cells. miR‐193a harboured negative correlation with NEAT1 and IL17RD expression in CRC specimens. In vivo experiment further validated the inhibitory effects of NEAT1 knockdown on xenograft tumour growth.ConclusionOur findings demonstrate that lncRNA NEAT1 acts as an oncogenic role in CRC cells by sponging miR‐193a and may represent a potential marker for CRC patients.
Highlights
Colorectal cancer (CRC) is one of the most common malignant dis‐ eases worldwide.[1]
We found that nuclear‐enriched abundant transcript 1 (NEAT1) expression was upregulated in CRC samples and was associated with TNM stage and poor prognosis, acting as an independent prognostic factor of tumour recurrence in patients with CRC
To understand the molecular mechanisms by which miR‐193a mediates the functions of NEAT1 in CRC cells, miR‐193a inhibitor and sh‐NEAT1 were co‐transfected into LOVO and HCT116 cell lines, indicating that miR‐193a inhibitor promoted cell proliferation and invasive potential, but knockdown of NEAT1 counteracted these tumour promoting effects induced by miR‐193a inhibitor (Figure 5A,B)
Summary
Colorectal cancer (CRC) is one of the most common malignant dis‐ eases worldwide.[1]. Endoscopic resection, more than 50% of CRC patients are found at an advanced stage and have poor survival and recurrence due to tumour invasiveness.[3] Colorectal tumorigenesis is caused by vari‐ ous factors in the complicated multi‐stage process involving the successive accumulation of genetic alterations. Identification of these potential biomarkers is indispensable for early detection and diagnosis of CRC. NEAT1 promoted the tumorigen‐ esis of CRC cells by sponging miR‐193a and represented a potential marker for CRC patients
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