A computational approach reveals the critical role of PARK2 gene and the potential infectious pathways and HPV infection in colorectal cancer

Colorectal cancer is a type of cancer that begins in the colon or rectum, and it is also known as colon cancer or rectal cancer, depending on where it begins. Colorectal cancer is one of the most common and deadly cancers, with a wide range of outcomes and medication responses. The human papillomavirus produces benign and malignant neoplasms in epidermal and mucosal epithelial cells. HPVs that are often found in anogenital malignancies, particularly cancers of the cervix and anus, are classified as high-risk or oncogenic. The PARK2 gene is one of the most important genes known to be linked to the ubiquitin proteasomal system and to play a role in cancer and other serious disorders. In order to comprehend the genotype-phenotype relationship in complicated disorders, high-throughput data (genomic and proteomic) is commonly collected. In this study, we focused on the relationship between the human papillomavirus, the PARK2 gene, gene expression patterns, altered genes, and their activities in colorectal cancer. We got the data from a publically available database for gene expression, mutations, and structural variants in human colorectal cancer for this study. We looked at it in terms of clinical importance by combining the Gene Expression Omnibus, TCGA, and ProteinAtlas datasets. According to our findings, the PARK2 gene impacts not only the ubiquitin proteasomal systems, but also key pathways, particularly those involved with the immune system, which may be directly responsible for colorectal and other types of cancer, as well as other key human disorders. Furthermore, it demonstrates that the HPV-infected genes and their estimated roles were potentially shared with genes that are important components of well-known colorectal cancer control and coordination pathways.