Abstract
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.
Highlights
Hepatocellular carcinoma (HCC) is one of the important types of cancer prevalent worldwide mainly in developing countries
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/βcatenin signaling pathways as potential target sites for Bromelain to arrest the progression of cancer
Summary
Hepatocellular carcinoma (HCC) is one of the important types of cancer prevalent worldwide mainly in developing countries. HCC is the third most common cause of fatality in cancer-related diseases throughout the world. It is estimated that around 600,000 deaths per year resulted due to the effective invasive nature of the HCC cells which enter into the metastatic stage. The patients diagnosed as an advanced stage in HCC state have a low survival rate as there are no suitable curative therapies for such patients. There is an urgent need in addressing the effective treatment options to treat HCC patients. Evaluating the underlying molecular mechanisms in HCC provides alternate therapeutic strategies which help in achieving more favorable clinical outcomes with less toxicity and thereby reducing the overall morbidity rates [1]
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