Received: 30-Nov-2022, Manuscript No. GJBBR-22-83805; Editor assigned: 02-Dec-2022, Pre QC No. GJBBR-22-83805(PQ); Reviewed: 16-Dec-2022, QC No. GJBBR-22-83805; Revised: 23-Dec-2022, Manuscript No. GJBBR-22-83805(R); Published: 30-Dec-2022, DOI: 10.15651/2504-001X.22.10.020
One of the most prevalent malignancies among males in the United States is Prostate Cancer (PCa), which accounts for 21% of newly diagnosed cancer cases and the second-leading cause of cancer death (an estimated 333300 deaths in 2020). Prostatectomy or radiation therapy will usually cure PCa in its early stages, but a tiny percentage of patients will progress to castration-resistant prostate cancer, which can metastasize fatally.
A basic understanding of the molecular pathways underlying the onset and development of PCa has been disclosed by a few researches. It was once believed that the recurrent TMPRSS2-ETS family fusion was mostly unique to prostate cancer. The 5'-untranslated region of TMPRSS2 was reported to be fused with ETS family genes, such as ERG, ETV1 and ETV4, to increase prostate cancer growth and invasion. Three other androgen responsive genes, SLC45A3, NDRG1, and HEPPUD1, were found to fuse with ERG in addition to TMPRSS2. In contrast to one study's finding that only 5%–10% of samples were fused with ETS, the incidence of ETS fusion in prostate cancer was as high as 70%.
Although Prostate-Specific Antigen (PSA) is a prostate tissue specific biomarker rather than a PCa specific one, it has been discovered to be increased in prostate cancer and is used as a good standard of diagnosis or screening the early-stage prostate cancer. PDGFR-β, HOX6C, ITPR3, Chromogranin A, and Sialyltransferase I are five genes that have been linked to a positive relationship with prostate cancer recurrence. Histone3 and Histone4 acetylation and demethylation in primary PCa may be used to predict recurrence independently of PSA level. Prostate cancer patients' prognoses were discovered to be substantially linked with EZH2, a component of polycomb repression group complexes.
A technique for analysing the gene co-expression network is called Weight Gene Co-expression Network Analysis (WGCNA). In order to identify the hub genes, it primarily groups together genes with similar expression into one module and connects the module with clinical features. Here, we primarily employed WGCNA and Gene Score Enrichment Analysis (GSEA) to uncover the molecular basis of the PCa pathogenic process, and we identified the PCa-related hub gene FERMT2. Cell biology tests revealed that FERMT2 prevented PC3's prostate cancer cell lines from proliferating and migrating. Potential biomarkers for PCa diagnosis and insight into the development of therapy strategies include FERMT2.
The main cause of morbidity and mortality in the US is Prostate Cancer (PCa), although it is still unclear how it develops on a molecular level. Here, by analysing PCa transcriptome data from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) datasets using bioinformatics methods, we found that the focal adhesion route was the primary problem pathway and that FERMT2 was the critical gene in prostate carcinogenesis.
Cell Adhesion Mediated Drug Resistance (CAMDR) and cell adhesion mediated radioresistance are two examples of how the focal adhesion pathway plays a significant role in carcinogenesis. The cytoplasmic signalling necessary for cell survival, proliferation, and motility is maintained by focal adhesion pathway proteins, which also participated in the ECM connection and contributed in cell morphology maintenance. ErbB2 and STAT3 were downregulated when 4 integrin, an adhesion molecule for ECM proteins, was reduced. This prevented the onset of breast cancer. While overexpression of α2β1 induced differentiation and decreased proliferation in breast cancer cells.