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      OncoTargets and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the pathological basis of cancers, potential targets for therapy and treatment protocols to improve the management of cancer patients. Publishing high-quality, original research on molecular aspects of cancer, including the molecular diagnosis, since 2008. Sign up for email alerts here. 50,877 Monthly downloads/views I 4.345 Impact Factor I 7.0 CiteScore I 0.81 Source Normalized Impact per Paper (SNIP) I 0.811 Scimago Journal & Country Rank (SJR)

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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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          Abstract

          Background

          Melanoma 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.

          Methods

          qRT-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.

          Results

          LncRNA 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.

          Conclusion

          Our work suggests that lncRNA CAR10 promotes melanoma growth and metastasis through modulating miR-125b-5p/RAB3D axis.

          Most cited references26

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          lncRNA JPX/miR-33a-5p/Twist1 axis regulates tumorigenesis and metastasis of lung cancer by activating Wnt/β-catenin signaling

          Jinchang Pan, Shuai Fang, Haihua Tian … (2020)
          Background MicroRNAs (miRNAs) and Twist1-induced epithelial-mesenchymal transition (EMT) in cancer cell dissemination are well established, but the involvement of long noncoding RNAs (lncRNAs) in Twist1-mediated signaling remains largely unknown. Methods RT-qPCR and western blotting were conducted to detect the expression levels of lncRNA JPX and Twist1 in lung cancer cell lines and tissues. The impact of JPX on Twist1 expression, cell growth, invasion, apoptosis, and in vivo tumor growth were investigated in lung cancer cells by western blotting, rescue experiments, colony formation assay, flow cytometry, and xenograft animal experiment. Results We observed that lncRNA JPX was upregulated in lung cancer metastatic tissues and was closely correlated with tumor size and an advanced stage. Functionally, JPX promoted lung cancer cell proliferation in vitro and facilitated lung tumor growth in vivo. Additionally, JPX upregulated Twist1 by competitively sponging miR-33a-5p and subsequently induced EMT and lung cancer cell invasion. Interestingly, JPX and Twist1 were coordinately upregulated in lung cancer tissues and cells. Mechanically, the JPX/miR-33a-5p/Twist1 axis participated in EMT progression by activating Wnt/β-catenin signaling. Conclusions These findings suggest that lncRNA JPX, a mediator of Twist1 signaling, could predispose lung cancer cells to metastasis and may serve as a potential target for targeted therapy.
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            Long noncoding RNA lncKdm2b is required for ILC3 maintenance by initiation of Zfp292 expression

            Benyu Liu, Buqing Ye, Liuliu Yang … (2017)
            Long noncoding RNAs contribute to the cell-type-specific regulation of gene expression. Fan and colleagues identify a unique conserved lncRNA, lncKdm2b, that is transcribed divergently from the Kdm2b gene and is necessary for ILC3 maintenance in the gut.
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              DNA-methylation-mediated activating of lncRNA SNHG12 promotes temozolomide resistance in glioblastoma

              Chenfei Lu, Yutian Wei, Xiefeng Wang … (2020)
              Background Accumulating evidence shows that long noncoding RNAs (lncRNAs) are important regulator molecules involved in diverse biological processes. Acquired drug resistance is a major challenge in the clinical treatment of glioblastoma (GBM), and lncRNAs have been shown to play a role in chemotherapy resistance. However, the underlying mechanisms by which lncRNA mediates TMZ resistance in GBM remain poorly characterized. Methods Quantitative reverse transcription PCR (qRT-PCR) and fluorescence in situ hybridization assays were used to detect small nucleolar RNA host gene 12 (SNHG12) levels in TMZ-sensitive and TMZ-resistant GBM cells and tissues. The effects of SNHG12 on TMZ resistance were investigated through in vitro assays (western blots, colony formation assays, flow cytometry assays, and TUNEL assays). The mechanism mediating the high expression of SNHG12 in TMZ-resistant cells and its relationships with miR-129-5p, mitogen-activated protein kinase 1 (MAPK1), and E2F transcription factor 7 (E2F7) were determined by bioinformatic analysis, bisulfite amplicon sequencing, methylation-specific PCR, dual luciferase reporter assays, chromatin immunoprecipitation assays, RNA immunoprecipitation assays, immunofluorescence, qRT-PCR, and western blot. For in vivo experiments, an intracranial xenograft tumor mouse model was used to investigate SNHG12 function. Results SNHG12 was upregulated in TMZ-resistant cells and tissues. Overexpression of SNHG12 led to the development of acquired TMZ resistance, while knockdown of SNHG12 restored TMZ sensitivity. An abnormally low level of DNA methylation was detected within the promoter region of SNHG12, and loss of DNA methylation made this region more accessible to the Sp1 transcription factor (SP1); this indicated that methylation and SP1 work together to regulate SNHG12 expression. In the cytoplasm, SNHG12 served as a sponge for miR-129-5p, leading to upregulation of MAPK1 and E2F7 and endowing the GBM cells with TMZ resistance. Disinhibition of MAPK1 regulated TMZ-induced cell apoptosis and the G1/S cell cycle transition by activating the MAPK/ERK pathway, while E2F7 dysregulation was primarily associated with G1/S cell cycle transition. Clinically, SNHG12 overexpression was associated with poor survival of GBM patients undergoing TMZ treatment. Conclusion Our results suggest that SNHG12 could serve as a promising therapeutic target to surmount TMZ resistance, thereby improving the clinical efficacy of TMZ chemotherapy.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Onco Targets Ther
                Journal ID (iso-abbrev): Onco Targets Ther
                Journal ID (publisher-id): OTT
                Journal ID (pmc): ott
                Title: OncoTargets and therapy
                Publisher: Dove
                ISSN (Electronic): 1178-6930
                Publication date (Electronic): 29 June 2020
                Publication date Collection: 2020
                Volume: 13
                Pages: 6203-6211
                Affiliations
                [1 ]Department of Dermatology, The Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People’s Hospital , Wenzhou 325000, People’s Republic of China
                [2 ]Department of Neurology, The Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital , Wenzhou 325000, People’s Republic of China
                [3 ]Department of Reproduction and Genetics, The Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital , Wenzhou 325000, People’s Republic of China
                [4 ]Department of Dermatology, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou 325000, People’s Republic of China
                Author notes
                Correspondence: Mingfen Lv Department of Dermatology, The First Affiliated Hospital of Wenzhou Medical University , Ouhai District, Wenzhou325000, People’s Republic of China Email mingfenlv@sina.com
                Article
                Publisher ID: 249736
                DOI: 10.2147/OTT.S249736
                PMC ID: 7334016
                PubMed ID: 32636644
                SO-VID: 421544b3-9c07-4db0-93fa-3e3dc1070bee
                Copyright © © 2020 Xie et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 14 February 2020
                Date accepted : 17 May 2020
                Page count
                Figures: 5, References: 32, Pages: 9
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: melanoma,car10,progression,mir-125b-5p,rab3d
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: melanoma, car10, progression, mir-125b-5p, rab3d

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