Answer:
The drugs will need to target the genes and proteins that are responsible for the process of mitosis, The drugs could target the promoter regions of proto-oncogenes, that spur mitosis, and make them inaccessible to RNA polymerase. This will reduce the number of cyclins D1 and CDK4 & CDK6 that ‘floor the gas pedal’ on mitosis. These cancer drugs could also increase the expression of tumor suppressor genes by RNA polymerase hence increasing the number of tumor suppressor proteins that ‘put the brakes’ on mitosis.
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Carcinogenesis is associated with the inactivation of tumor suppressor genes. These genes are involved in different cellular pathways such as programmed cell death and cell cycle arrest.
Tumor suppressor genes are a broad category of genes involved in slowing down cell proliferation, repair DNA errors (mutations), or indicate the time when programmed cell death (i.e., apoptosis) takes place.
In cancer cells, tumor suppressor genes are often inactivated, thereby cancer cells can bypass cellular pathways above cited.
Therefore, cancer cells acquire resistance to apoptosis and/or cell cycle arrest pathways.
Programmed cell death is mediated by caspase enzymes that drive apoptosis by cleaving specific proteins during the cell cycle.
On the other hand, different kinase enzymes (e.g., ATM kinase) are involved in normal cell proliferation by promoting the phosphorylation of tumor suppressor proteins (e.g., P53, H2AX, and BRCA1), which are involved in cell cycle arrest.
In consequence, the development of drugs designed to induce the activation of caspase and kinase genes could then be used to prevent the proliferation of cancer cells.
In conclusion, tumor suppressor genes are inactivated in cancer pathways, thereby the restoration of the normal functions of these genes can be used to prevent the proliferation of cancer cells.
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