Molecular pathogenesis, mechanism and therapy of Cav1 in prostate cancer

Abstract

Prostate cancer is the second incidence of malignant tumors in men worldwide. Its incidence and mortality are increasing year by year. Enhanced expression of Cav1 in prostate cancer has been linked to both proliferation and metastasis of cancer cells, influencing disease progression. Dysregulation of the Cav1 gene shows a notable association with prostate cancer. Nevertheless, there is no systematic review to report about molecular signal mechanism of Cav1 and drug treatment in prostate cancer. This article reviews the structure, physiological and pathological functions of Cav1, the pathogenic signaling pathways involved in prostate cancer, and the current drug treatment of prostate cancer. Cav1 mainly affects the occurrence of prostate cancer through AKT/mTOR, H-RAS/PLCε, CD147/MMPs and other pathways, as well as substance metabolism including lipid metabolism and aerobic glycolysis. Baicalein, simvastatin, triptolide and other drugs can effectively inhibit the growth of prostate cancer. As a biomarker of prostate cancer, Cav1 may provide a potential therapeutic target for the treatment of prostate cancer.

CAV1 and KRT5 are potential targets for prostate cancer

“…Abnormal Cav1 expression leads to faster progression of prostate cancer and is not conducive to treatment. [27] The above literature review is consistent with our results, and based on above literature analysis, we speculate that CAV1 may play an important role in occurrence and development of prostate cancer, but its mechanism of action on prostate cancer needs to be further explored.…”

CD147/Basigin Is Involved in the Development of Malignant Tumors and T-Cell-Mediated Immunological Disorders via Regulation of Glycolysis

“…On the other hand, the silencing of MCT-4 impaired the maturation and trafficking of CD147 to the cell surface, resulting in the accumulation of CD147 in the endoplasmic reticulum [49]. Recent studies revealed the involvement of CD147 in cancer cell glycolysis in various malignant tumors including non-small-cell lung cancer, hepatocellular carcinoma, colorectal cancer, prostate cancer, and anaplastic large-cell lymphoma [50][51][52][53][54][55]. These findings strongly suggest that CD147 interacts with MCT-1 and MCT-4 to promote glycolysis in tumor cells, resulting in tumor progression (Figure 2).…”