LncRNA-RMRP promotes carcinogenesis by acting as a miR-206 sponge and is used as a novel biomarker for gastric cancer

Shao, Yongfu; Ye, Meng; Li, Qier; Sun, Weiliang; Zhang, Xinjun; Yang, Yingzhen; Xiao, Bingxiu; Guo, Junming

doi:10.18632/oncotarget.9336

Cited by 162 publications

(142 citation statements)

References 39 publications

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“…Previous study showed that RMRP increased aggressive gastric cancer by regulating Cyclin D2 as the ceRNA for miR-206 [31]. In line with this, we demonstrated that overexpression of RMRP suppressed miR-206 expression in lung adenocarcinoma cell.…”

Section: Discussionsupporting

confidence: 89%

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LncRNA-RMRP Acts as an Oncogene in Lung Cancer

Meng

Ren

et al. 2016

PLoS ONE

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Accumulating studies have demonstrated that long noncoding RNAs (lncRNAs) act a crucial role in the development of tumors. However, the role of lncRNAs in lung cancer remains largely unknown. In this study, we demonstrated that theexpression of RMRP was upregulated in lung adenocarcinoma tissues compared to the matched adjacent normal tissues. Moreover, of 35 lung adenocarcinoma samples, RMRP expression was upregulated in 25 cases (25/35; 71.4%) compared to the adjacent normal tissues. We also showed that RMRP expression was upregulated in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) compared to the bronchial epithelial cell line (16HBE). Ectopic expression of RMRP promoted lung adenocarcinoma cell proliferation, colony formation and invasion. In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer. These data suggested that RMRP might serve as a therapeutic target in lung adenocarcinoma.

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Section: Discussionsupporting

confidence: 89%

“…Previous study showed that the expression of RMRP was deregulated in gastric cancer [30]. Moreover, Shao et al [31]. showed that RMRP expression level was downregulated in gastric cancer tissues and gastric dysplasia.…”

Section: Introductionmentioning

confidence: 99%

LncRNA-RMRP Acts as an Oncogene in Lung Cancer

Meng

Ren

et al. 2016

PLoS ONE

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“…Over the past decade, small non-coding RNAs, such as miRNAs, have been extensively studied, and their roles in gene regulation and cell function have been elucidated in numerous cancers [23-27]. Recent studies have indicated that lncRNA also participate in several different biologic processes and play oncogenic or tumor suppressive roles during tumorigenesis [28-30]. However, the roles of lncRNAs in NSCLC remain largely unknown.…”

Section: Discussionmentioning

confidence: 99%

The Long Non-Coding RNA XIST Controls Non-Small Cell Lung Cancer Proliferation and Invasion by Modulating miR-186-5p

Wang

Shen

Zhang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Long non-coding RNAs (lncRNAs) are key players in the development and progression of human cancers. The lncRNA XIST (X-inactive specific transcript) has been shown to be upregulated in human non-small cell lung cancer (NSCLC); however, its role and molecular mechanisms in NSCLC cell progression remain unclear. Methods: qRT-PCR was conducted to assess the expression of XIST and miR-186. Cell proliferation was detected using MTT assay. Cell invasion and migration were evaluated using transwell assay. Cell cycle distribution and apoptosis rates were analyzed by flow cytometry. Luciferase reporter assay was used to identify the direct regulation of XIST and miR-186. A RNA immunoprecipitation was used to analyze whether XIST was associated with the RNA-induced silencing complex (RISC). Results: We confirmed that XIST was upregulated in NSCLC cell lines and tissues. Functionally, XIST knockdown inhibited cancer cell proliferation and invasion, and induced apoptosis in vitro, and suppressed subcutaneous tumor growth in vivo. Mechanistic investigations revealed a reciprocal repressive interaction between XIST and miR-186-5p. Furthermore, we showed that miR-186-5p has a binding site for XIST. Our data also indicated that XIST and miR-186-5p are likely in the same RNA induced silencing complex. Conclusion: Together, our data revealed that XIST knockdown confers suppressive function in NSCLC and XIST may be a novel therapeutic marker in this disease.

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“…MALAT1 modulates TGF-β1-induced endothelial-to-mesenchymal transition (EndMT) of endothelial progenitor cells through regulation of TGFBR2 and SMAD3 via miR-145 [17]. RMRP promotes carcinogenesis and serves as a novel biomarker for gastric cancer [18]. RP11-708H21.4 is down-regulated in colorectal cancer (CRC) samples, while its upregulation blocked AKT/mTOR pathway and repressed in vivo CRC xenograft tumor growth [19].…”

Section: Introductionmentioning

confidence: 99%

Microarray Profiling of TGF-β1-Induced Long Non-Coding RNA Expression Patterns in Human Lung Bronchial Epithelial BEAS-2B Cells

Pei

Zhu

et al. 2018

Cell Physiol Biochem

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Background/Aims: TGF-β1 mediated radiation-induced bystander effects (RIBE) have been linked with malignant transformation and tumorigenesis. However, the underlying mechanisms are not fully understood. Methods: To reveal new molecules of regulatory functions in this process, lncRNA microarray was performed to profile both lncRNA and mRNA expression patterns in human lung bronchial epithelial BEAS-2B cells treated with TGF-β1 at a concentration measured in the medium conditioned by directly irradiated BEAS-2B cells. The potential functions of the differentially expressed lncRNAs were predicted by GO and KEGG pathway analyses of their co-expressed mRNAs. Cis- and trans-regulation of the lncRNAs were analyzed and the interaction networks were constructed using Cytoscape. qRT-PCR was conducted to validate the results of microarray profiling. CCK-8 assay was employed for functional validation of 3 identified lncRNAs. Results: 224 lncRNAs were found to be dysregulated, among which 6 lncRNAs were chosen for expression validation by qRT-PCR assay. Pathway analyses showed that differentially expressed lncRNAs are highly correlated with cell proliferation, transformation, migration, etc. Trans-regulation analyses showed that the differentially expressed lncRNAs most likely participate in the pathways regulated by four transcriptional factors, FOS, STAT3, RAD21 and E2F1, which have been identified to be involved in the modulation of oncogenic transformation, cell cycle progression, genomic instability, etc. lnc-THEMIS-2 and lnc-ITGB6-4, predicted to be regulated by STAT3 and E2F1 respectively, were found to rescue the decrease of cell viability induced by TGF-β1 treatment. Conclusion: Our findings suggest that the differentially expressed lncRNAs induced by TGF-β1 play crucial roles in the oncogenic transformation and tumorigenesis, which provide a better understanding of the underlying mechanisms related to tumorigensis induced by LD/LDR radiations.

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LncRNA-RMRP promotes carcinogenesis by acting as a miR-206 sponge and is used as a novel biomarker for gastric cancer

Cited by 162 publications

References 39 publications

LncRNA-RMRP Acts as an Oncogene in Lung Cancer

LncRNA-RMRP Acts as an Oncogene in Lung Cancer

The Long Non-Coding RNA XIST Controls Non-Small Cell Lung Cancer Proliferation and Invasion by Modulating miR-186-5p

Microarray Profiling of TGF-β1-Induced Long Non-Coding RNA Expression Patterns in Human Lung Bronchial Epithelial BEAS-2B Cells

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