NOP7 interacts with &amp;beta;-catenin and activates &amp;beta;-catenin/TCF signaling in hepatocellular carcinoma cells

Wu, Nan; Zhao, Jing; Yuan, Youhua; Lu, Chuanjia; Zhu, Wenjing; Jiang, Qun

doi:10.2147/ott.s164601

Cited by 5 publications

(10 citation statements)

References 20 publications

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“…The studies showed that activation of the Wnt/β-catenin signaling pathway, interaction, and stabilization of β-catenin and TCF is important. PES1 gene is involved in this process through β-catenin/TCF signaling stabilizes the interaction of β-catenin and TCF [13]. The same type of study revealed that CARF is also involved in the stabilization process between β-catenin and TCF where CARF blocks ICAT from binding to β-catenin and helps β-catenin to interact with TCF [14].…”

Section: Murthy and Narsaiahmentioning

confidence: 91%

Bioinformatics Approach on Action and Mechanism of Bromelain in Hepatocellular Carcinoma

Murthy

2021

Asian J Pharm Clin Res

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Objective: The objective of the study was to understand biomolecular interactions of Bromelain and its networking with p53 and β-catenin by a computational method of analysis in Hepatocellular carcinoma (HCC) condition. Methodology: The protein interaction partners for p53 and β-catenin involved in the progression of HCC were collected from National Center for Biotechnology Information. We collected data points and standardized the data points for our data analysis from the public database. We used Cytoscape 3.8.2 version plug-in for constructing a Protein-Protein interaction network. We constructed a pathway network using Biorender.com. Results: The protein interactions concerning p53 and β-catenin are identified and a network is constructed. A total of 18 and 34 nodes were identified which are involved in down-regulation and up-regulation of β-catenin and a total of 30 and 27 nodes for homosapiens are identified which are involved in the downregulation and upregulation of the p53 gene. We identified different pathways which trigger and impact the p53 and Wnt/β- catenin signaling pathways as potential target sites for Bromelain to arrest the progression of cancer Conclusion: In conclusion, our in silico studies anti-cancer activity of Bromelain in HCC relating its effect on apoptosis, cell differentiation, mesenchymal transition, p53 signaling, and Wnt/β-catenin signaling pathways.

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Section: Murthy and Narsaiahmentioning

confidence: 91%

Bioinformatics Approach on Action and Mechanism of Bromelain in Hepatocellular Carcinoma

Murthy

2021

Asian J Pharm Clin Res

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“…PES1 promoted the proliferation, migration, invasion and tumorigenesis of liver cancer cells [14,[16][17][18]. After knocking down PES1, the expression of Ki67 protein decreased, the number of cells was significantly reduced and the growth of liver cancer cells in mice was decreased [17].…”

Section: Hepatocellular Carcinoma (Hcc)mentioning

confidence: 99%

“…Furthermore, Wei et al found that CD44 regulates PES1 by regulating the expression of miR-105-5p, thereby promoting the proliferation of liver cancer cells [15]. Wu et al reported that the protein levels of N-cadherin, snail, vimentin and cyclin D1 were down-regulated after PES1 knockdown [18]. Cyclin D1 is a downstream gene of the β-Catenin/TCF complex, which indicates that PES1 can activate the βcatenin/TCF signaling pathway.…”

Section: Hepatocellular Carcinoma (Hcc)mentioning

confidence: 99%

“…A large number of studies have shown that PES1 is related to tumor cell proliferation, invasion and metastasis of multiple types of cancer, including prostate cancer [12,13], liver cancer [14][15][16][17][18], pancreatic cancer [19], papillary thyroid cancer (PTC) [20], breast cancer [21][22][23][24], ovarian cancer [25], gastric cancer (GC) [26], neuroblastoma [27], colon cancer [28], and others. There are also some studies showing that PES1 is related to the prognosis of some cancers [14,28].…”

Section: Introductionmentioning

confidence: 99%

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The functional role of Pescadillo ribosomal biogenesis factor 1 in cancer

Li¹,

Zhang²,

Pei³

et al. 2022

J. Cancer

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Tumors are neogrowths formed by the growth of normal cells or tissues through complex mechanisms under the influence of many factors. The occurrence and development of tumors are affected by many factors. Pescadillo ribosomal biogenesis factor 1 (PES1) has been identified as a cancer-related gene. The study of these genes may open up new avenues for early diagnosis, treatment and prognosis of tumors. As a nucleolar protein and part of the Pes1/Bop1/WDR12 (PeBoW) complex, PES1 is involved in ribosome biogenesis and DNA replication. Many studies have shown that high expression of PES1 is often closely related to the occurrence, proliferation, invasion, metastasis, prognosis and sensitivity to chemotherapeutics of various human malignant tumors through a series of molecular mechanisms and signaling pathways. The molecules that regulate the expression of PES1 include microRNA (miRNA), circular RNA (circRNA), c-Jun, bromodomain-containing protein 4 (BRD4) and nucleolar phosphoprotein B23. However, the detailed pathogenic mechanisms of PES1 overexpression in human malignancies remains unclear. This article summarizes the role of PES1 in the carcinogenesis, prognosis and treatment of multiple tumors, and introduces the molecular mechanisms and signal transduction pathways related to PES1.

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“…Therefore, it is speculated that it is the key molecule in the HBV-HCC process, which needs further exploration. On the other hand, NOP7 interacts with beta-catenin to activate the inflammatory signaling pathway of beta-catenin/TCF, and its upregulation promotes the proliferation and migration of HCC cancer cells[17]. To some extent, these results indicate that HBV may mediate the occurrence and development of HCC, and guide a comprehensive and in-depth discussion on the bridge mechanism between them.…”

Section: Introductionmentioning

confidence: 99%

Identification of hepatitis B virus and liver cancer bridge molecules based on functional module network

Huang

Feng

et al. 2019

WJG

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BACKGROUNDThe potential role of chronic inflammation in the development of cancer has been widely recognized. However, there has been little research fully and thoroughly exploring the molecular link between hepatitis B virus (HBV) and hepatocellular carcinoma (HCC).AIMTo elucidate the molecular links between HBV and HCC through analyzing the molecular processes of HBV-HCC using a multidimensional approach.METHODSFirst, maladjusted genes shared between HBV and HCC were identified by disease-related differentially expressed genes. Second, the protein-protein interaction network based on dysfunctional genes identified a series of dysfunctional modules and significant crosstalk between modules based on the hypergeometric test. In addition, key regulators were detected by pivot analysis. Finally, targeted drugs that have regulatory effects on diseases were predicted by modular methods and drug target information.RESULTSThe study found that 67 genes continued to increase in the HBV-HCC process. Moreover, 366 overlapping genes in the module network participated in multiple functional blocks. It could be presumed that these genes and their interactions play an important role in the relationship between inflammation and cancer. Correspondingly, significant crosstalk constructed a module level bridge for HBV-HCC molecular processes. On the other hand, a series of non-coding RNAs and transcription factors that have potential pivot regulatory effects on HBV and HCC were identified. Among them, some of the regulators also had persistent disorders in the process of HBV-HCC including microRNA-192, microRNA-215, and microRNA-874, and early growth response 2, FOS, and Kruppel-like factor 4. Therefore, the study concluded that these pivots are the key bridge molecules outside the module. Last but not least, a variety of drugs that may have some potential pharmacological or toxic side effects on HBV-induced HCC were predicted, but their mechanisms still need to be further explored.CONCLUSIONThe results suggest that the persistent inflammatory environment of HBV can be utilized as an important risk factor to induce the occurrence of HCC, which is supported by molecular evidence.

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NOP7 interacts with β-catenin and activates β-catenin/TCF signaling in hepatocellular carcinoma cells

Cited by 5 publications

References 20 publications

Bioinformatics Approach on Action and Mechanism of Bromelain in Hepatocellular Carcinoma

Bioinformatics Approach on Action and Mechanism of Bromelain in Hepatocellular Carcinoma

The functional role of Pescadillo ribosomal biogenesis factor 1 in cancer

Identification of hepatitis B virus and liver cancer bridge molecules based on functional module network

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