Dataset Information

LncRNA MCM3AP-AS1 Upregulates CDK4 by Sponging miR-545 to Suppress G1 Arrest in Colorectal Cancer.

ABSTRACT: Introduction:This study aimed to investigate the role of lncRNA MCM3AP-AS1 in colorectal cancer (CRC). Methods:Paired tumor and non-tumor tissues were collected from 60 CRC patients. Expression of MCM3AP-AS1 was determined by RT-qPCR. Overexpression of MCM3AP-AS1, miR-545, and CDK4 in CRC cells was achieved to explore the interactions between them. Cell cycle assay was performed to analyze the roles of MCM3AP-AS1, miR-545, and CDK4 in regulating the cell cycle progression of CRC cells. Results:We found that MCM3AP-AS1 was upregulated in CRC and its high expression levels predicted poor survival of CRC patients. MCM3AP-AS1 is predicted to interact with miR-545. In CRC cells, overexpression of MCM3AP-AS1 and miR-545 was achieved, while their overexpression did not affect the expression of each other. Instead, overexpression of MCM3AP-AS1 led to the increased expression levels of CDK4, which is a downstream target of miR-545. Cell cycle analysis showed that overexpression of MCM3AP-AS1 and CDK4 suppressed G1 arrest induced by miR-545. In addition, overexpression of MCM3AP-AS1 reduced the enhancing effects of overexpressing miR-545 on cell cycle progression. Conclusion:MCM3AP-AS1 may upregulate CDK4 by sponging miR-545 to induce G1 arrest in CRC cells.

SUBMITTER: Ma X

PROVIDER: S-EPMC7494958 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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LncRNA MCM3AP-AS1 Upregulates CDK4 by Sponging miR-545 to Suppress G1 Arrest in Colorectal Cancer.

Ma Xudong X Luo Jing J Zhang Yi Y Sun Dali D Lin Yueying Y

Cancer management and research 20200907

<h4>Introduction</h4>This study aimed to investigate the role of lncRNA MCM3AP-AS1 in colorectal cancer (CRC).<h4>Methods</h4>Paired tumor and non-tumor tissues were collected from 60 CRC patients. Expression of MCM3AP-AS1 was determined by RT-qPCR. Overexpression of MCM3AP-AS1, miR-545, and CDK4 in CRC cells was achieved to explore the interactions between them. Cell cycle assay was performed to analyze the roles of MCM3AP-AS1, miR-545, and CDK4 in regulating the cell cycle progression of CRC c ...[more]

PMID: 32982409

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Project description:Long non-coding RNAs (lncRNAs) play a crucial role in tumor generation and progression. However, the exact functional significance and underlying molecular mechanism by which lncRNA CERS6-AS1 operates in the context of lung adenocarcinoma (LUAD) remain unknown. We aimed to evaluate the potential role of the CERS6-AS1/miR-424-5p/ANLN axis in the progression of LUAD through bioinformatics and cytobehavioral experiments, and to provide a new insight into the combined treatment of LUAD. Based on the TCGA database, the expression of CERS6-AS1 in pan-cancer was evaluated, and its prognostic performance in LUAD was evaluated by ROC curve, survival curve and COX analysis. In addition, quantification of CERS6-AS1 expression levels in LUAD patients and lung cancer cells using quantitative real-time polymerase chain reaction (RT-qPCR), and further validate the functional significance of CERS6-AS1 in promoting the proliferation, migration, and invasion abilities of lung cancer cells. The competitive endogenous RNA (ceRNA) network was constructed, and miR-424-5p inhibitors were applied to CERS6-AS1 knockdown cells. The potential downstream genes associated with the regulatory axis of CERS6-AS1/miR-424-5p were analyzed by PPI network and gene enrichment analysis (KEGG). Finally, we evaluated the prognostic value of high expression of ANLN in LUAD and its effects on immune cell infiltration, tumor mutation burden, chemotherapy response, and immunotherapy. CERS6-AS1 expression was significantly elevated in both LUAD patients and lung cancer cells. In the CERS6-AS1 knockdown assay, the proliferation, invasion, migration and epithelial-mesenchymal transformation (EMT) of cancer cells were significantly inhibited. Notably, there was a prominent upregulation of miR-424-5p expression in cells where CERS6-AS1 was knocked down. Co-transfection of siRNA and miR-424-5p inhibitors into lung cancer cells restored the restriction on lung cancer cells. Anillin (ANLN) has been identified as a potential target gene for miR-424-5p and as a prognostic and immune biomarker associated with immune cell infiltration and tumor mutational burden in LUAD. Additionally, ANLN impacts the efficacy of chemotherapy and immunotherapy in LUAD patients. This study reveals a novel regulatory mechanism in which CERS6-AS1 may contribute to the progression of LUAD by influencing the expression of ANLN as a competitive sponge for miR-424-5p.

Dataset Information

LncRNA MCM3AP-AS1 Upregulates CDK4 by Sponging miR-545 to Suppress G1 Arrest in Colorectal Cancer.

Publications

LncRNA MCM3AP-AS1 Upregulates CDK4 by Sponging miR-545 to Suppress G1 Arrest in Colorectal Cancer.

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