Silencing of a novel lncRNA LOC105369748 suppresses the progression of hepatocellular carcinoma by sponging miR‐5095 from MBD2

Changyong, E; Li, Chunsheng; Li, Hang; Yang, Jinghui

doi:10.1002/jcp.28486

Cited by 4 publications

(4 citation statements)

References 26 publications

(38 reference statements)

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“…24 LOC105369748 upregulates MBD2 through binding to miR-5095, which conveys oncogenic signals to accelerate the carcinogenesis and progression of hepatocellular carcinoma. 25 All above evidence indicates an oncogenic role of MBD2 in the initiation and progression of cancers. However, the pathophysiologic function and regulatory mechanism of MBD2 in RCC remain largely unknown.…”

Section: Introductionmentioning

confidence: 94%

“…Aberrant DNA methylation modifications are frequently detected in various tumors, and the main mechanisms for DNA methylation-involved tumorigenesis are that methylation levels of the promoter region of anti-oncogene are elevated, which promotes the key anti-oncogene silencing and drives tumorigenesis. 12,[14][15][16] MBD2 has been reported in multiple human malignancies, including gastric cancer, 17 breast cancer, 18,19 colorectal cancer, 20 glioblastoma, 21,22 hilar cholangiocarcinoma, 23 hepatocellular carcinoma, 24,25 chronic myeloid leukemia 26 and prostate cancer. 27 Previous studies confirmed that MBD2 mediates the transcriptional repression of tumor suppressor genes, such as hTERT, 28 GSTP1, 29 BAI1, 21 p14 ARF /p16 INK4a,30 and 14-3-3sigma, 27 which supports the pivotal role of MBD2 in abnormal epigenetic regulation of tumors.…”

Section: Introductionmentioning

confidence: 99%

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<p>MBD2 Correlates with a Poor Prognosis and Tumor Progression in Renal Cell Carcinoma</p>

Li¹,

Li²,

Liu³

et al. 2020

OTT

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DNA methylation plays an important role in regulating gene expression. Methyl-CpG-binding domain (MBD) proteins recognize and bind to methylated DNA, which mediate gene silencing by the interaction with deacetylases and histone methyltransferases. MBD2 has been reported in various human cancers; however, its clinical implication and potential regulatory role in renal cell carcinoma (RCC) have not been elaborated. Materials and Methods: In the study, we estimated the expression and prognostic value of MBD2 in RCC cell lines and tissues by Western blotting and immunohistochemistry. The associations of MBD2 expression and pathological characters and survival in RCC patients were performed using χ2 and Kaplan-Meier survival analysis, respectively. Univariate and multivariable Cox regression analyses suggested the independent predictors in RCC prognosis. The functional role of MBD2 in RCC progression was assessed by in vitro cell experiments. In addition, we identified the MBD2-mediated alterations of protein-related proliferation and EMT markers in RCC cells after MBD2 overexpression and knockdown. Results: We found that the protein levels of MBD2 were upregulated in RCC cells and tissues. High MBD2 expression was related to TNM stage and predicted poorer survival in RCC. Enforced expression of MBD2 significantly promoted the proliferation, cycle progress, invasion and migration of RCC cells in vitro. However, downregulating MBD2 remarkably weakened the above cell functions. Mechanistically, the promotive effect of MBD2 overexpression may be regulated by its effects onp21, p53 and Cyclin D1 expression and EMT process. Conclusion: These results indicated that MBD2confers an oncogenic function in the malignant progression of RCC. MBD2 could be served as a meaningful prognostic biomarker and a latent therapeutic target in RCC patients.

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Section: Introductionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

<p>MBD2 Correlates with a Poor Prognosis and Tumor Progression in Renal Cell Carcinoma</p>

Li¹,

Li²,

Liu³

et al. 2020

OTT

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“…Therefore, maximum radical resection of the tumor and reduction of residual cancer tissue are essential to improve the prognosis of HGSOC. In addition, the expression level of MBD2 in HCC is higher compared with that in normal tissues ( 51 ). MBD2 is an independent prognostic factor that affects the overall survival and disease-free survival of patients and is considered to be a potential clinical prognostic marker ( 17 ).…”

Section: Discussionmentioning

confidence: 99%

Expression and clinical significance of methyl‑CpG binding domain protein 2 in high‑grade serous ovarian cancer

Gong

Chen

et al. 2020

Oncol Lett

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Platinum resistance is an important cause of clinical recurrence and mortality of patients with high-grade serous ovarian cancer (HGSOC). Methyl-CpG binding domain protein 2 (MBD2) serves an important role in tumor progression; however, its role in HGSOC remains unclear. The aim of the present study was to investigate the expression of MBD2 in HGSOC and its role in drug resistance and prognosis of HGSOC. MBD2 expression was analyzed by immunohistochemical staining and western blotting. The associations between MBD2 expression and clinical pathological features, platinum resistance and patient prognosis were analyzed using a χ 2 test, Kaplan-Meier analysis and Cox regression analysis. Positive MBD2 expression was detected in 73 (63.5%) of the HGSOC tissue samples, whereas it was undetectable in all 16 normal tissue samples (100%) analyzed, indicating a significantly higher expression level in tumor tissues compared with normal tissues (P<0.001). Additionally, MBD2 expression was significantly higher in platinum-resistant cases compared with that in platinum-sensitive cases (P<0.05). In addition, high expression of MBD2 was negatively associated with relapse-free survival (P<0.05). In conclusion, MBD2 was demonstrated to be a potential drug target and a biomarker for poor prognosis in HGSOC. WANGANG GONG 1-4 , MAOWEI NI 2-4 , ZHONGBO CHEN 2-4 and ZHIGUO ZHENG 2-4

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“…Recent reports have unveiled several lncRNAs that play oncogenic or tumor-suppressive roles in HCC. For instance, a lncRNA named LOC105369748 was found to overexpress in HCC tissues and further promote the proliferation, migration, invasion, and epithelial-to-mesenchymal transition of HCC cells [10]. Similarly, FLVCR1 antisense RNA 1 (FLVCR1-AS1) is another lncRNA was reported to be up-regulated in HCC tissues.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA RP11-284P20.2 promotes cell proliferation and invasion in hepatocellular carcinoma by recruiting EIF3b to induce c-met protein synthesis

et al. 2020

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A newly identified lncRNA designated as RP11-284P20.2 has been identified to be up-regulated in hepatocellular carcinoma (HCC), but its role in HCC remain poorly understood. Quantitative PCR and immunocytochemical analysis were performed using the HCC tissues to identify the potential interaction partners of RP11-284P20.2. Moreover, RP11-284P20.2 was knocked down in HCC cell lines, HepG2 and SMMC7721, to investigate the influence of this lncRNA on cell growth properties. Additionally, RNA fluorescence in situ hybridization and immunofluorescence, RNA immunoprecipitation, and RNA pull-down assays were performed to determine the interaction of RP11-284P20.2 with c-met mRNA and eukaryotic translation initiation factor 3b (EIF3b). Silencing RP11-284P20.2 inhibited cell viability, migration, invasion, and colony formation, and increased apoptosis. Overexpression of c-met abolished these effects of RP11-284P20.2 in HCC cells. Histopathological examination showed that HCC tissues with high RP11-284P20.2 expression had higher c-met protein level than that in HCC tissues with low RP11-284P20.2 expression. However, there was no positive correlation between the expression levels of RP11-284P20.2 and c-met mRNA. RP11-284P20.2 knockdown led to a decease in c-met protein expression level, but did not affect the c-met mRNA expression level. These data suggest that RP11-284P20.2 regulates c-met protein expression level, which is independent of c-Met mRNA expression level. It was also confirmed that RP11-284P20.2 has high affinity toward both c-met mRNA and EIF3b protein, and hence RP11-284P20.2 probably recruits EIF3b protein to c-met mRNA and further facilitates its translation. RP11-284P20.2 promotes cell proliferation and invasion in hepatocellular carcinoma by recruiting EIF3b to induce c-met protein synthesis.

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Silencing of a novel lncRNA LOC105369748 suppresses the progression of hepatocellular carcinoma by sponging miR‐5095 from MBD2

Cited by 4 publications

References 26 publications

<p>MBD2 Correlates with a Poor Prognosis and Tumor Progression in Renal Cell Carcinoma</p>

<p>MBD2 Correlates with a Poor Prognosis and Tumor Progression in Renal Cell Carcinoma</p>

Expression and clinical significance of methyl‑CpG binding domain protein 2 in high‑grade serous ovarian cancer

Long non-coding RNA RP11-284P20.2 promotes cell proliferation and invasion in hepatocellular carcinoma by recruiting EIF3b to induce c-met protein synthesis

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