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MiR-30a-3p inhibits renal cancer cell invasion and metastasis through targeting ATG12.

ABSTRACT: Correspondence to: Yonghui Chen; Wei Xue. Department of Urology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China. Email: cyh1488@163.com; xuewei@renji.com. Background:Aberrantly expressed microRNAs play important biological functions in the pathogenesis, progression and metastasis of numerous malignancies. Thus, further identification of these non-coding transcriptions is warranted. Methods:miRNAs expression data of renal cell carcinoma (RCC) as well as the normal renal tissue samples was downloaded from TCGA and GEO database, and was analyzed by both computational and experimental approaches. The bio-functional role of the miRNA was then moreover identified by over-expression and inhibition assays. Beyond that, Western blots, luciferase assays, along with immunohistochemistry (IHC) tests were conducted for further study of the potential mechanisms. Results:In this study, a novel regulatory miRNA, miR-30a-3p, was identified along with its biological function as well as prognostic value in RCC. Functionally, miR-30a-3p inhibits RCC cell invasion and migration. miR-30a-3p targets autophagy related 12 (ATG12), which we confirmed by luciferase reporter assays and Western blotting. Conclusions:In conclusion, miR-30a-3p, as a new prognostic marker in RCC, down-regulates RCC cell invasion and migration by targeting ATG12. This consistently improves the overall survival of RCC patients.

SUBMITTER: Chen Y

PROVIDER: S-EPMC7214999 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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miR-30a-3p inhibits renal cancer cell invasion and metastasis through targeting ATG12.

Chen Yonghui Y Zhou Jiale J Wu Xiaorong X Huang Jiwei J Chen Wei W Liu Dongming D Zhang Jin J Huang Yiran Y Xue Wei W

Translational andrology and urology 20200401 2

<i>Correspondence to:</i> Yonghui Chen; Wei Xue. Department of Urology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China. Email: cyh1488@163.com; xuewei@renji.com.<h4>Background</h4>Aberrantly expressed microRNAs play important biological functions in the pathogenesis, progression and metastasis of numerous malignancies. Thus, further identification of these non-coding transcriptions is warranted.<h4>Methods</h4>miRNAs expression data of renal cell carcino ...[more]

PMID: 32420171

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Project description:BackgroundMicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression, influence cellular processes, and promote disease development. Variations in miRNA expression have been observed in many diseases, including hepatitis, cardiovascular disease, and cancer. The aim of this study is to investigate the effect of miR-144-3p on the invasion and metastasis of lung adenocarcinoma by targeting recombinant insulin receptor substrate 1 (IRS1).MethodsThe expression of miR-144-3p in patients with lung adenocarcinoma was queried through bioinformatics database. MirTarPathway was used to analyze the KEGG enrichment pathway of miRNA. The expression and plasmid transfection efficiency of miR-144-3p in lung adenocarcinoma cell lines were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Transwell assay was used to detect the changes of cell invasion and migration ability in different groups. Bioinformatics determined the key genes (Hub genes) of miR-144-3p; Double luciferase target assay was used to detect the mutual binding of miR-144 and IRS1. Western blot assay was used to detect the expression of IRS1 in different cell lines and the expression of after overexpression of miR-144.ResultsThe expression of miR-144-3p in lung adenocarcinoma tissues was decreased, qRT-PCR results indicated that the expression of miR-144-3p in lung adenocarcinoma cell A549 was significantly decreased (P<0.05), and the overexpressed plasmid was successfully transfected (P<0.05). Overexpression of miR-144 decreased the ability of cell migration and invasion (P<0.05). The expression of IRS1 was up-regulated in lung adenocarcinoma tissues. Survival analysis showed that patients with lung adenocarcinoma with high IRS1 expression had a poor prognosis (P<0.05). Double luciferase assay results showed that miR-144 could specifically identify 3'-UTR of IRS1 and inhibit reporter enzyme expression (P<0.05). Western blot indicated that the expression of IRS1 was increased in A549 cells (P<0.05). After overexpression of miR-144, the expression level of IRS1 protein was decreased (P<0.05). Transwell experiment proved that miR-144-3p could inhibit invasion and metastasis of lung adenocarcinoma cells by targeting IRS1 (P<0.05).ConclusionsMiR-144-3p inhibits the invasion and migration of A549 cells through targeted regulation of IRS1, thus playing an anticancer role in tumors.

Project description:Objective:Mounting research has established the role of microRNAs (miRNAs) as oncogenes or anti-oncogenes (tumor suppressors) in the development and progression of several cancers. The purpose of our current study is to delineate the roles and functional mechanisms of miR-331-3p and MLLT10 in non-small cell lung cancer (NSCLC) tumorigenesis. Patients and Methods:Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was employed to measure miR-331-3p expression levels in twenty-six matched tumor tissues and non-cancerous tissues collected from patients suffering from NSCLC, and from six NSCLC cell lines separately: A549, H1650, H292, H1299, H1944 and BEAS-2b. We employed the dual-luciferase activity assay to check whether the putative gene, MLLT10, was a downstream target of miR-331-3p in NSCLC pathogenesis and development. Western blot was conducted to analyze the protein expression levels of MLLT10 (AF10), E-cadherin, Vimentin, and GAPDH. CCK-8 assay, transwell migration assay, and transwell invasion assay were carried out to observe the functions of miR-331-3p and MLLT10 on NSCLC tumor cell proliferation, metastasis, and invasion, respectively. To identify whether the metastasis of NSCLC tumor cells was EMT-mediated, supplementary experiments involving E-cadherin and Vimentin were implemented. Results:miR-331-3p was downregulated in NSCLC, which promoted tumor cell proliferation, whereas the overexpression of miR-331-3p inhibited tumor cell proliferation. Being a direct target of miR-331-3p, MLLT10 was negatively modulated by miR-331-3p, which suppressed tumor cell proliferation, migration, and invasion in NSCLC. However, MLLT10 overexpression alleviated the above inhibitory effects. Furthermore, EMT-mediated metastasis was proved to be present in NSCLC. Conclusion:miR-331-3p played a suppressor role in NSCLC tumor cell proliferation, EMT-mediated metastasis, and invasion by targeting MLLT10. Our findings highlighted that miR-331-3p/MLLT10 axis could be useful as a clinical diagnostic marker and therapeutic target in NSCLC patients.

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MiR-30a-3p inhibits renal cancer cell invasion and metastasis through targeting ATG12.

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miR-30a-3p inhibits renal cancer cell invasion and metastasis through targeting ATG12.

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