A gene module identification algorithm and its applications to identify gene modules and key genes of hepatocellular carcinoma

Zhang, Yan; Lin, Zhengkui; Lin, Xiaofeng; Zhang, Xue; Zhao, Qian; Sun, Yeqing

doi:10.1038/s41598-021-84837-y

Cited by 13 publications

(12 citation statements)

References 51 publications

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“…23 As a result of various studies, CCNB1 is believed to be overexpressed in HCC. 21,22,24–30 However, a large sample size is needed to verify the expression patterns of CCNB1 in HCC, and the mechanisms of CCNB1 in HCC are still unknown. Moreover, the potential clinical implications of CCNB1 expression in HCC patients need to be further studied.…”

Section: Introductionmentioning

confidence: 99%

CCNB1 promotes the development of hepatocellular carcinoma by mediating DNA replication in the cell cycle

Rong

Zhong

et al. 2021

Exp Biol Med (Maywood)

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In our studies, cyclin B1 ( CCNB1) mRNA and protein were overexpressed in hepatocellular carcinoma (HCC) tissues compared with non-HCC tissues. Moreover, CCNB1 was overexpressed in the serum of HCC patients. The expression of CCNB1 was associated with several crucial clinicopathologic characteristics, and the HCC patients with overexpressed CCNB1 had worse overall survival outcomes. In the screening of interactional genes, a total of 266 upregulated co-expression genes, which were positively associated with CCNB1, were selected from the datasets, and 67 downregulated co-expression genes, which were negatively associated with CCNB1, were identified. The key genes might be functionally enriched in DNA replication and the cell cycle pathways. CDC20, CCNA2, PLK1, and FTCD were selected for further research because they were highly connected in the protein-protein interaction networks. Upregulated CDC20, CCNA2, and PLK1 and downregulated FTCD might result in undesirable overall survival outcomes for HCC patients. The univariate Cox analysis results showed that CDC20 and PLK1 might be two independent risk factors, while FTCD might be protective in HCC. Therefore, CCNB1 may participate in the cell cycle of HCC by regulating DNA replication, and CCNB1 may provide a direction for the diagnosis of early-stage HCC and targeted HCC therapy.

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Section: Introductionmentioning

confidence: 99%

CCNB1 promotes the development of hepatocellular carcinoma by mediating DNA replication in the cell cycle

Rong

Zhong

et al. 2021

Exp Biol Med (Maywood)

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“…WGCNA has the advantage of computing complex network relationships but suffers from the disadvantage of ignoring modularity in module identification process and no flexibility to adjust the algorithm in the calculation. For the important role of modularity in network clustering and community detection, high modularity raising more reliable clustering results ( 62 ). Considering that WGCNA cannot identify modules with overlapping genes.…”

Section: Discussionmentioning

confidence: 99%

Integration of Molecular Inflammatory Interactome Analyses Reveals Dynamics of Circulating Cytokines and Extracellular Vesicle Long Non-Coding RNAs and mRNAs in Heroin Addicts During Acute and Protracted Withdrawal

Zhang

Wu²,

Peng³

et al. 2021

Front. Immunol.

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Heroin addiction and withdrawal influence multiple physiological functions, including immune responses, but the mechanism remains largely elusive. The objective of this study was to investigate the molecular inflammatory interactome, particularly the cytokines and transcriptome regulatory network in heroin addicts undergoing withdrawal, compared to healthy controls (HCs). Twenty-seven cytokines were simultaneously assessed in 41 heroin addicts, including 20 at the acute withdrawal (AW) stage and 21 at the protracted withdrawal (PW) stage, and 38 age- and gender-matched HCs. Disturbed T-helper(Th)1/Th2, Th1/Th17, and Th2/Th17 balances, characterized by reduced interleukin (IL)-2, elevated IL-4, IL-10, and IL-17A, but normal TNF-α, were present in the AW subjects. These imbalances were mostly restored to the baseline at the PW stage. However, the cytokines TNF-α, IL-2, IL-7, IL-10, and IL-17A remained dysregulated. This study also profiled exosomal long non-coding RNA (lncRNA) and mRNA in the plasma of heroin addicts, constructed co-expression gene regulation networks, and identified lncRNA-mRNA-pathway pairs specifically associated with alterations in cytokine profiles and Th1/Th2/Th17 imbalances. Altogether, a large amount of cytokine and exosomal lncRNA/mRNA expression profiling data relating to heroin withdrawal was obtained, providing a useful experimental and theoretical basis for further understanding of the pathogenic mechanisms of withdrawal symptoms in heroin addicts.

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“…Moreover, NOP56 is significantly correlated with the survival prognosis, pathological stage, immune infiltration, and tumor progression of patients with hepatocellular carcinoma, and may be used as a target for the diagnosis and treatment of hepatocellular carcinoma in the future. The methylation analysis indicated that the hypomethylation of the NOP56 promoter may lead to the overexpression of NOP56, which proved that expression of NOP56 may be a potential biomarker of hepatocellular carcinoma (66,67). In hepatocellular carcinoma, NOP56 is considered as a potential immune marker associated with HBV virus, which can be processed and presented by antigenpresenting cells (APCs) to induce immune responses.…”

Section: Nop56 and Hepatocellular Carcinomamentioning

confidence: 99%

The roles of NOP56 in cancer and SCA36

Zhao¹,

Zhang²,

Liu³

et al. 2023

Pathol. Oncol. Res.

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NOP56 is a highly conserved nucleolar protein. Amplification of the intron GGCCTG hexanucleotide repeat sequence of the NOP56 gene results in spinal cerebellar ataxia type 36 (SCA36). NOP56 contains an N-terminal domain, a coiled-coil domain, and a C-terminal domain. Nucleolar protein NOP56 is significantly abnormally expressed in a number of malignant tumors, and its mechanism is different in different tumors, but its regulatory mechanism in most tumors has not been fully explored. NOP56 promotes tumorigenesis in some cancers and inhibits tumorigenesis in others. In addition, NOP56 is associated with methylation in some tumors, suggesting that NOP56 has the potential to become a tumor-specific marker. This review focuses on the structure, function, related signaling pathways, and role of NOP56 in the progression of various malignancies, and discusses the progression of NOP56 in neurodegenerative and other diseases.

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A gene module identification algorithm and its applications to identify gene modules and key genes of hepatocellular carcinoma

Cited by 13 publications

References 51 publications

CCNB1 promotes the development of hepatocellular carcinoma by mediating DNA replication in the cell cycle

CCNB1 promotes the development of hepatocellular carcinoma by mediating DNA replication in the cell cycle

Integration of Molecular Inflammatory Interactome Analyses Reveals Dynamics of Circulating Cytokines and Extracellular Vesicle Long Non-Coding RNAs and mRNAs in Heroin Addicts During Acute and Protracted Withdrawal

The roles of NOP56 in cancer and SCA36

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