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Long Noncoding RNA CAR10 Contributes to Melanoma Progression By Suppressing miR-125b-5p to Induce RAB3D Expression.

ABSTRACT: BackgroundMelanoma is a very malignant skin cancer with high mortality and unsatisfactory prognosis. Many long noncoding RNAs (lncRNAs) have been reported to be aberrantly expressed in melanoma. How lncRNA regulates melanoma progression is poorly defined. LncRNA CAR10 has been shown to regulate the progression of several cancers and its role in melanoma remains unclear. This study aims to determine the role and mechanism of lncRNA CAR10 in the regulation of melanoma progression.MethodsqRT-PCR was utilized to analyze CAR10 in melanoma human tissues and cell lines while Kaplan–Meier curve was used to examine the survival rate. CCK8 assay and EdU assay were used to assess cell proliferation when Transwell assay was conducted to determine migration and invasion. And tumor xenograft assay was performed to evaluate tumor growth in vivo. Additionally, luciferase assay and RNA pulldown assay were performed to analyze the interactions among CAR10, miR-125b-5p and RAB3D.ResultsLncRNA CAR10 was upregulated in melanoma tissues and cell lines. Upregulation of CAR10 predicted a poor prognosis in patients with melanoma. CAR10 knockdown suppressed proliferation, migration and invasion of melanoma cells in vitro. CAR10 silencing attenuated tumor growth in vivo. CAR10 inhibited miR-125b-5p activity to upregulate RAB3D expression. And miR-125b-5p/RAB3D signaling is crucial for CAR10-dependent melanoma progression.ConclusionOur work suggests that lncRNA CAR10 promotes melanoma growth and metastasis through modulating miR-125b-5p/RAB3D axis.

SUBMITTER: Xie J

PROVIDER: S-EPMC7334016 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Project description:BackgroundmiR-488-3p has been reported to play an important role in cancer progression and metastasis. The protein 53 (P53) gene serves as a mediator and biomarker of esophageal squamous cell carcinoma (ESCC). However, the molecular mechanism underlying miR-488-5p in the pathology of ESCC through the P53 pathway has not been examined.MethodsThe expression levels of miR-488-5p were determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Cytological experiments were performed to evaluate the biological functions of miR-488-5p. A bioinformatics analysis was performed to determine the pathways and key miR-488-5p targets associated with ESCC. Correlations between miR-488-5p and P53 signaling pathways were validated by western blotting and the dual luciferase reporter gene system. Finally, the expression level of miR-488-5p was regulated and tumor formation experiments were performed in nude mice.ResultsThe qRT-PCR analysis showed that MiR-488-5p expression was more upregulated in the KYSE-150 group than the HEEC group. In the KYSE-150 cells, the colony formation assay and flow cytometry analysis indicated that the miR-488-5p inhibitor inhibited cell viability and increased cell apoptosis; however, these effects were recovered by P53 knockdown (KD). In addition, cell invasion and cell migration were inhibited by the miR-488-5p inhibitor, but were also improved by P53 KD. Similarly, the miR-488-5p inhibitor induced the expression of P53 and P21 than normal control (NC) group in which miR-488-5p expression was normal, while P53 KD prevented the effects of the miR-488-5p inhibitor in KYSE-150 cells. Additionally, we found that tumor size was obviously smaller in miR-488-5p overexpression (OE)+ P53 OE mice than miR-488-5p OE mice. Hematoxylin and eosin and immunohistochemistry staining also revealed similar results.ConclusionsOur results suggest that miR-488-5p promotes ESCC progression by suppressing the P53 pathway. These findings should provide novel ideas for ESCC therapies.

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Long Noncoding RNA CAR10 Contributes to Melanoma Progression By Suppressing miR-125b-5p to Induce RAB3D Expression.

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