Dataset Information

Knockdown of LINC01614 inhibits lung adenocarcinoma cell progression by up-regulating miR-217 and down-regulating FOXP1.

ABSTRACT: We tried to identify the function of LINC01614 in lung adenocarcinoma (LUAD) and reveal its underlying mechanisms. qRT-PCR was applied to assess the expression of LINC016014 in LUAD tissues, noncancerous tissues and cells. Through colony formation assay, MTT assay and apoptosis analysis, we examined the variation of cell proliferation and apoptosis ability after silencing LINC01614. Moreover, the targeting interactions among LINC01614, miR-217 and FOXP1 were validated via luciferase reporter assay, and then, we regulated the expression of miR-217 and FOXP1 to ascertain their importance in cell proliferation and apoptosis. LINC01614 and FOXP1 were found to be up-regulated in LUAD tumours and cells, whereas miR-217 was down-regulated. The experiment showed that target-specific selectivity exists between LINC01614-miR-217 and miR-217-FOXP1 3'UTR. Furthermore, we disclosed that inhibition of LINC01614 could activate miR-217, which subsequently restrained FOXP1. It was proved that LINC01614 promoted FOXP1 by inhibiting miR-217, which ultimately stimulated the development of LUAD.

SUBMITTER: Liu AN

PROVIDER: S-EPMC6111824 | biostudies-other | 2018 Sep

REPOSITORIES: biostudies-other

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Knockdown of LINC01614 inhibits lung adenocarcinoma cell progression by up-regulating miR-217 and down-regulating FOXP1.

Liu Ai-Na AN Qu Hua-Jun HJ Yu Cai-Yan CY Sun Ping P

Journal of cellular and molecular medicine 20180622 9

We tried to identify the function of LINC01614 in lung adenocarcinoma (LUAD) and reveal its underlying mechanisms. qRT-PCR was applied to assess the expression of LINC016014 in LUAD tissues, noncancerous tissues and cells. Through colony formation assay, MTT assay and apoptosis analysis, we examined the variation of cell proliferation and apoptosis ability after silencing LINC01614. Moreover, the targeting interactions among LINC01614, miR-217 and FOXP1 were validated via luciferase reporter ass ...[more]

PMID: 29934982

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Project description:BackgroundColorectal cancer (CRC) poses a heavy threat to human health owing to its high incidence and mortality. Circular RNAs (circRNAs) were investigated to participate in the progression of CRC, whereas there was no revenant data on the CRC process regulated by hsa_circ_0000231. This study aimed to explore the effects of hsa_circ_0000231 on CRC progression and underneath regulatory mechanism.MethodsThe expression levels of hsa_circ_0000231, miR-502-5p, and Myosin VI (MYO6) mRNA were detected by quantitative real time polymerase chain reaction (qRT-PCR). Western blot was employed to determine the protein expression levels of MYO6 and proliferating cell nuclear antigen (PCNA). The effects of hsa_circ_0000231 on cell proliferation, apoptosis, migration, and invasive in CRC were determined by cell counting kit-8 proliferation (CCK-8) and colony formation assays, flow cytometry analysis, wound-healing assay, and transwell invasion assay, respectively. Glucose uptake and lactate production were severally illustrated by glucose assay kit and lactate assay kit. The relationship between miR-502-5p and hsa_circ_0000231 or MYO6 was predicted by circular RNA interactome or targetScan online databases, and identified by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. In vivo tumor formation assay was carried out to determine the effects of hsa_circ_0000231 knockdown on tumor growth in vivo.ResultsHsa_circ_0000231 expression was dramatically upregulated while miR-502-5p was obviously downregulated in CRC tissues and cells compared with control groups. Hsa_circ_0000231 knockdown repressed the expression levels of MYO6 and PCNA protein. Functionally, hsa_circ_0000231 knockdown repressed cell glycolysis, proliferation, migration and invasion, and induced cell apoptosis, whereas these effects were decreased by miR-502-5p inhibitor. Mechanistically, hsa_circ_0000231 acted as a sponge of miR-502-5p and miR-502-5p bound to MYO6. Furthermore, hsa_circ_0000231 knockdown decreased tumor volume and weight of CRC in vivo.ConclusionHsa_circ_0000231 knockdown inhibited CRC progression and glycolysis by downregulating MYO6 expression through sponging miR-502-5p, which might provide a theoretical basis in further studying circ_0000231-directed therapy in CRC.

Dataset Information

Knockdown of LINC01614 inhibits lung adenocarcinoma cell progression by up-regulating miR-217 and down-regulating FOXP1.

Publications

Knockdown of LINC01614 inhibits lung adenocarcinoma cell progression by up-regulating miR-217 and down-regulating FOXP1.

Similar Datasets

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