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LncRNA DGCR 5/miR-27a-3p/BNIP3 promotes cell apoptosis in pancreatic cancer by regulating the p38 MAPK pathway.

ABSTRACT: Long non-coding RNA (lncRNA) DGCR5 has been identified as a tumor suppressor in several types of cancer. However, its biological functions in pancreatic cancer (PaCa) have not yet been fully elucidated. The present study was designed to investigate the role of lncRNA DGCR5 in the regulation of PaCa cell apoptosis. For this purpose, lncRNA DGCR5, miR-27a-3p and Bcl-2/adenovirus E1B-19kDa-interacting protein 3 (BNIP3) expression levels were examined by reverse transcription-quantitative (RT-qPCR) and western blot analysis, respectively. RNA pull-down assay was used to verify DGCR5 as a target of miR-27a-3p and dual luciferase reporter assay was used to clarify whether miR-27a-3p targets the BNIP3 3? UTR. In addition, PaCa cell apoptosis was assessed by flow cytometry. Recombinant plasmids and cell transfection were performed to modulate the endogenous expression of related genes. Thereafter, the role of DGCR5 in PaCa was analyzed using a nude mouse model of PaCa. lncRNA DGCR5 was found to be downregulated in PaCa tissues and cells. DGCR5 functioned as a decoy of miR-27a-3p, and BNIP3 was negatively regulated by miR-27a-3p. Following the transfection of DGCR5 plasmid into PaCa cells, the expression of miR-27a-3p was downregulated, and this downregulation was reversed following transfection with miR-27a-3p mimic. In addition, DGCR5 regulated the BNIP3 and p38 MAPK pathways via miR-27a-3p and promoted PaCa cell apoptosis via the miR-27a-3p/BNIP3 pathway. The results of in vivo experiments also indicated the positive effects of DGCR5 on a nude mouse model of PaCa. On the whole, the findings of the present study indicate that lncRNA DGCR5 upregulates the BNIP3 and p38 MAPK pathways via miR-27a-3p to promote PaCa cell apoptosis, thereby attenuating PaCa development.

SUBMITTER: Li X

PROVIDER: S-EPMC7307863 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Project description:BackgroundGastric cancer (GC) is one of the most common malignancies around the world. Recently, the role of long non-coding RNA (lncRNA) in cancer biology has become a hot research topic. This work aimed to explore the biological function and underlying mechanism of LINC01089 in GC.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) was employed to investigate the expression of LINC01089 in GC tissues and cells. The relationship between the expression level of LINC01089 and the clinicopathological parameters of GC was assessed. Cell models of LINC01089 overexpression, LINC01089 knockdown, miR-27a-3p overexpression, and miR-27a-3p inhibition were established by transfection. CCK-8 assay, BrdU assay, and Transwell assay were utilized to investigate the malignant biological behaviors of GC cell lines after transfection. Dual luciferase activity reporter assay, Pearson's correlation analysis, and Western blot were utilized to the regulatory relationships among LINC01089, miR-27a-3p and tet methylcytosine dioxygenase 1 (TET1).ResultLINC01089 down-regulation was observed in GC tissues and cell lines. Low expression level of LINC01089 in GC tissues was markedly linked to larger tumor size, higher T stage, as well as lymphatic metastasis of the patients. Functional experiments implied that LINC01089 overexpression impeded the proliferation, migration, as well as invasion of GC cells, whereas LINC01089 knockdown promoted the above malignant phenotypes. Additionally, up-regulation of miR-27a-3p was also observed in GC tissues. Functional experiments also showed that, miR-27a-3p overexpression boosted the malignant biological behaviors of GC cells; on the contrast, these phenotypes were impeded by miR-27a-3p inhibition. Moreover, LINC01089 interacted with and repressed miR-27a-3p, and miR-27a-3p antagonized the impact of LINC01089 on GC cells. Additionally, TET1 was verified as a target gene of miR-27a-3p, and could be positively regulated by LINC01089.ConclusionLINC01089 impedes the proliferation, migration, and invasion of GC cells by adsorbing miR-27a-3p and up-regulating the expression of TET1.

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LncRNA DGCR 5/miR-27a-3p/BNIP3 promotes cell apoptosis in pancreatic cancer by regulating the p38 MAPK pathway.

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