miR-331-3p, miR-338-3p, hsa-let-7b-3p, and HSF2 regulate MSRB3 expression and ROS-mediated apoptosis in cervical cancer; insights from bioinformatics study

Cervical cancer is one of the most common cancers in women and is the third leading cause of cancer-related mortality. Metabolic dysregulation is a common hallmark of cancer. Reactive-oxygen-species(ROS) are oxygen metabolism byproducts that are impacted by metabolic instability. ROS can trigger cellular apoptosis as a safety switch by controlling the intrinsic mitochondrial apoptosis pathway. MSRB3(methionine sulfoxide reductase B3) can inhibit ROS-mediated-apoptosis in cervical cancer cells,promoting tumorigenesis and metastasis. In this article,the effect of miR-331-3p,and miR-338-3p on reducing gene expression is investigated.The unfavorable proteins in cervical cancer tissues were selected and obtained using the Human-Protein-Atlas(HPA) database. OncoDB was used to find differentially-expressed-genes(DEGs) linked with the cancer stage. STRING database was used to predict functional interactions of human proteins with specific genes. The upstream transcription factor, Gene Ontology analysis, and potential mechanism of MSRB3 and its interacting proteins were all investigated using Enrichr. HPA identified 223 genes linked with poor prognosis in cervical cancer patients. OncoDB was used to identify the top 1,000 DEGs related to cervical cancer patients' clinical stages. MSRB3 expression was shown to be correlated with cervical cancer patient survival and clinical stage. A tight relationship between MSRB3 expression and ROS was discovered by Reactome.According to STRING, MSRB3 interacts with two additional genes (TXN(Thioredoxin) and FXN(Frataxin)). According to GO analysis, these genes were engaged in protein-repair pathways and had oxidoreductase-activity. We discovered that MSRB3 expression is associated with poor prognosis in cervical cancer patients. Using the miRWalk database,we predicted that the miR-331-3p, miR-338-3p, and hsa-let-7b-3p have the potential to be involved in regulating MSRB3 Also, due to the TRRUST analysis, HSF2 is an upstream transcription factor of MSRB3, TXN, and FXN can be knocked down in order to suppress MSRB3 with two additional genes. Thus, treatment strategies that target MSRB3 expression may prone cervical cancer cells to apoptosis.