Expression of the Long Intergenic Non-Protein Coding RNA 665 (LINC00665) Gene and the Cell Cycle in Hepatocellular Carcinoma Using The Cancer Genome Atlas, the Gene Expression Omnibus, and Quantitative Real-Time Polymerase Chain Reaction

Wen, Dong‐Yue; Lin, Peng; Pang, Yu‐Yan; Chen, Gang; He, Yun; Dang, Yi‐Wu; Yang, Hong

doi:10.12659/msm.907389

Cited by 47 publications

(49 citation statements)

References 41 publications

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“…Cell cycle protein A2 (CCNA2) is encoded by the CCNA2 gene in humans. CCNA2 is expressed in cell division and interacts with CDK kinase to regulate cell cycle progression [41]. The CCNA2-CDK complex may promote tumorigenesis by phosphorylation of cancer proteins or tumor suppressor genes, such as p53.…”

Section: Discussionmentioning

confidence: 99%

Joint bioinformatics analysis of underlying potential functions of hsa-let-7b-5p and core genes in human glioma

Chu

Liu

et al. 2019

J Transl Med

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Background: Glioma accounts for a large proportion of cancer, and an effective treatment for this disease is still lacking because of the absence of specific driver molecules. Current challenges in the treatment of glioma are the accurate and timely diagnosis of brain glioma and targeted treatment plans. To investigate the diagnostic biomarkers and prospective role of miRNAs in the tumorigenesis and progression of glioma, we analyzed the expression of miRNAs and key genes in glioma based on The Cancer Genome Atlas database. Methods: Of the 701 cases that were downloaded, five were normal and 696 were glioma. Then, 1626 differentially expressed genes were identified, and 173 aberrantly expressed miRNAs were calculated by edgeR. GO and KEGG pathway enrichment analyses were performed using Cytoscape software. A coexpression network was built by weighted correlation network analysis (WGCNA). A cell scratch test and transwell, cell apoptosis and cell cycle assays were performed to validate the function of hsa-let-7b-5p. Results: Based on crosstalk genes in the KEGG, PPI network, and WGCNA analyses, PLK1, CCNA2, cyclin B2 (CCNB2), and AURKA were screened as candidate diagnostic marker genes. The survival analysis revealed that high mRNA expression of PLK1, CCNA2, and AURKA was significantly associated with poor overall survival. Furthermore, hsalet-7b-5p was identified as a core miRNA in the regulation of candidate genes involved in glioma development. We confirmed that hsa-let-7b-5p could inhibit the migration, invasion, and cell cycle of glioma cells. Conclusions: This study provides four potential biomarkers for the diagnosis of glioma, offers a potential explanation of its pathogenesis, and proposes hsa-let-7b-5p as a therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Joint bioinformatics analysis of underlying potential functions of hsa-let-7b-5p and core genes in human glioma

Chu

Liu

et al. 2019

J Transl Med

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“…The process of qRT-PCR has been described in detail in previous studies. [17][18][19] GAPDH served as the reference gene for MIR22HG. Information about the primers for MIR22HG and GAPDH is listed in Table 1.…”

Section: Clinico-pathological Significance Of Mir22hg In Hccmentioning

confidence: 99%

“…Information about the primers for MIR22HG and GAPDH is listed in Table 1. 18,19 MIR22HG expression was calculated by the formula:…”

Section: Clinico-pathological Significance Of Mir22hg In Hccmentioning

confidence: 99%

<p>MIR22HG As A Tumor Suppressive lncRNA In HCC: A Comprehensive Analysis Integrating RT-qPCR, mRNA-Seq, And Microarrays</p>

Xiong

et al. 2019

OTT

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Introduction: MIR22HG has a reported involvement in the tumorigenesis of a variety of cancers, including hepatocellular carcinoma (HCC). However, the exact molecular mechanism of MIR22HG in HCC has not been clarified. Methods: In the present study, we integrated data from in-house RT-qPCR, RNA-sequencing, microarray, and literature studies to conduct a comprehensive evaluation of the clinicopathological and prognostic significance of MIR22HG in an extremely large group of HCC samples. We also explored the potential mechanism of MIR22HG in HCC by analyzing the alteration profiles of MIR22HG in HCC to predict transcription factors (TFs) that may interact with MIR22HG and to annotate the biological functions of genes co-expressed with MIR22HG. MIR22HG expression was also compared in HCC nude mice xenografts before and after a treatment with nitidine chloride. Results: We found that MIR22HG was downregulated in HCC and that this downregulation correlated with the malignant phenotype of HCC. Comprehensive analysis of the prognostic impact of MIR22HG in HCC revealed a beneficial effect of MIR22HG on the survival outcome of HCC patients. Seven cases of MIR22HG deep deletion occurred in 360 of the cancer genome atlas (TCGA) provisional HCC samples. A total of 22 MIR22HG-TF-mRNA triplets in HCC were predicted by the lncRNAmap. Co-expressed genes of MIR22HG, identified by weighted correlation network analysis (WGCNA), mainly participated in the pathways involving osteoclast differentiation, chemokine signaling pathways, and hematopoietic cell lineage. In vivo experiments demonstrated that nitidine chloride could stimulate MIR22HG expression in HCC xenografts. Conclusion: In summary, MIR22HG may play a tumor-suppressive role in HCC by coordinating with predicted TFs and co-expressed genes, such as NLRP3, CSF1R, SIGLEC10, and ZEB2, or by being controlled by nitidine chloride.

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“…The function of BUB1 as oncogene or tumor suppressor gene has been observed in various types of cancer, including breast cancer, pancreatic ductal adenocarcinoma, prostate and gastric cancer (12)(13)(14)(15). Several studies have demonstrated the unfavorable prognostic role of BUB1 in liver cancer based on bioinformatics analysis (16)(17)(18). However, the molecular biological function of BUB1 in liver cancer still remains unclear.…”

Section: Introductionmentioning

confidence: 99%

BUB1 promotes proliferation of liver cancer cells by activating SMAD2 phosphorylation

Zhu¹,

Pan²,

Chen

et al. 2020

Oncol Lett

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Budding uninhibited by benzimidazoles 1 (BUB1) is a mitotic checkpoint serine/threonine kinase that has been reported as an oncogene or tumor suppressor gene in various types of cancer, including breast cancer, pancreatic ductal adenocarcinoma, prostate and gastric cancers. However, its role in liver cancer remains unclear. The present study aimed to explore the biological function of BUB1 in liver cancer. The present study demonstrated that BUB1 mRNA expression levels and the intensity of immunohistochemical staining were significantly increased in liver cancer tissues compared with normal tissues. The role of BUB1 in cell proliferation was also determined. Overexpression of BUB1 significantly promoted cell proliferation, whereas knockdown of BUB1 expression inhibited the proliferation of liver cancer cell lines. In experiments investigating the underlying mechanism, overexpression of BUB1 increased the levels of SMAD2 phosphorylation, whereas knockdown of BUB1 reduced the levels of SMAD2 phosphorylation. Therefore, BUB1 may promote proliferation of liver cancer cells by activating phosphorylation of SMAD2, and BUB1 may serve as a potential target in the diagnosis and/or treatment of liver cancer.

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Expression of the Long Intergenic Non-Protein Coding RNA 665 (LINC00665) Gene and the Cell Cycle in Hepatocellular Carcinoma Using The Cancer Genome Atlas, the Gene Expression Omnibus, and Quantitative Real-Time Polymerase Chain Reaction

Cited by 47 publications

References 41 publications

Joint bioinformatics analysis of underlying potential functions of hsa-let-7b-5p and core genes in human glioma

Joint bioinformatics analysis of underlying potential functions of hsa-let-7b-5p and core genes in human glioma

<p>MIR22HG As A Tumor Suppressive lncRNA In HCC: A Comprehensive Analysis Integrating RT-qPCR, mRNA-Seq, And Microarrays</p>

BUB1 promotes proliferation of liver cancer cells by activating SMAD2 phosphorylation

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