Circular RNA cMras inhibits lung adenocarcinoma progression via modulating miR‐567/PTPRG regulatory pathway

Abstract

Objectives: Circular RNA, a type of RNA formed by a covalently closed loop, possesses sophisticated abilities of gene regulation in tumorigenesis and metastasis.However, the role of circRNAs on lung adenocarcinoma (LUAD) remains largely unknown. Materials and methods:The role of cMras was examined both in vitro and in vivo.cMras expression in LUAD tissues was determined by quantitative real-time PCR (qRT-PCR). Downstream targets of cMras were predicted by bioinformatics tools and confirmed by RNA immunoprecipitation assay and luciferase assay. qRT-PCR and western blot assay were used to detect the expression of specific targets.Results: Thirty-six paired LUAD and healthy tissues were collected and cMras resulted significantly downregulated in cancerous tissues. Its expression was negatively associated with tumour stages. cMras overexpression suppressed LUAD growth and metastasis, while endogenous cMras silencing resulted in the opposite effects. Bioinformatics analysis and experimental evidence confirmed that cMras was a sponge of miRNA-567 and released its direct target, PTPRG. cMras overexpression decreased miR-567 expression and subsequently increased PTPRG expression, while increased miRNA-567 expression blocked the effects induced by cMras.Moreover, PTPRG was downregulated in LUAD and patients with low PTPRG expression exhibited significantly poor prognosis. These results suggested that cMras/ miR-567/PTPRG regulatory pathway might be associated to LUAD tumorigenesis and development. Conclusions:A novel circular RNA cMras and its functions were identified, discovering a cMras/miR-567/PTPRG regulatory pathway in LUAD tumorigenesis and development.

DDIAS promotes STAT3 activation by preventing STAT3 recruitment to PTPRM in lung cancer cells

“…The known STAT3-binding phosphatases are receptor-type PTPs such as PTPRK, PTPRD, and PTPRK and nonreceptor PTPs, including SHP1, SHP2, PTP-MEG2, and TC-PTP. These PTPs are frequently mutated or inactivated in lung cancer, colorectal cancer, glioblastoma, head and neck squamous cell carcinomas, and renal cell carcinoma 21,23,24,[44][45][46] , suggesting that their inactivation contributes to the malignancy of human cancers.…”

A novel circRNA, circNUP98, a potential biomarker, acted as an oncogene via the miR‐567/ PRDX3 axis in renal cell carcinoma

“…In line with previous studies, our data also indicated that miR‐567 might be a tumour suppressor in RCC cells. Noteworthy, a recent study reported that miR‐567 could be sponged by circRNA cMars and inhibition of miR‐567 contributed to the progression of lung adenocarcinoma 23 . This discrepancy might be caused by different tumour tissues, thereby more investigations regarding the function of miR‐567 are necessary.…”

Identification of a 5-Gene Metabolic Signature for Predicting Prognosis Based on an Integrated Analysis of Tumor Microenvironment in Lung Adenocarcinoma

“…Patients could have totally different final outcomes although they might possess similar clinical and pathological types [ 20 ]. The development of next-generation sequencing promoted the preclinical application of bioinformatics [ 21 , 22 ], which could comprehensively combine the gene profiling with the clinical parameters. Compared with the tumor-node-metastasis (TNM) system, it has been confirmed among various types of cancers that the prognostic signature could improve the accuracy of prediction [ 23 – 25 ].…”