What are the oncogenes and tumor suppressor genes related to ovarian cancer

Ovarian cancer is a common and highly prevalent malignant tumor in gynecology. Its pathogenic factors are not only related to heredity, diet, industrial exposure, etc., but also the result of multi-stage interaction of oncogenes and tumor suppressor genes related to cell proliferation and differentiation. It has been found that oncogenes such as K-ras, C-myc, C-erb-B2 and tumor suppressor genes such as p53 and p16 are closely related to ovarian cancer. Understanding the relationship between these genes and ovarian cancer is conducive to the formulation of a reasonable gene therapy plan.

The K-ras encoded protein is activated through point mutation, causing it to lose its guanosine triphosphate (GPT) kinase activity, slowing down the degradation of GTP into guanosine diphosphate (GDP). Continuous activation of target molecules can cause cells to continue to proliferate, leading to cell cancer.

c-myc encodes a transcription factor. If C-myc continues to proliferate and overexpress, it may lose its gene transcription and control capabilities, causing cells to proliferate and induce cancer.

C-erb-B2 encodes a cell surface protein with a structure similar to that of epidermal growth factor receptor, which plays an important role in the occurrence of breast cancer and ovarian cancer.

The p53 gene is the most intensively studied tumor suppressor gene. It can monitor the integrity of the normal cell genome. If the DNA is damaged, the p53 gene will cause cell division to arrest at the G phase through the transcriptional regulation mechanism, allowing the cells to have enough time to repair the damage. About 30% to 80% of ovarian cancer patients have p53 mutations, which undoubtedly increases the chance of cell canceration.

The p16 tumor suppressor gene is a gene directly involved in cell cycle regulation. It competitively binds to cyclin-dependent kinase (CDK4) with cyclins, thereby inactivating CDK4 and preventing cells from entering the S phase from the G phase, thereby inhibiting cell division and preventing them from developing in a malignant direction.