Chapter 11.6, Problem 15SAQ

Summary Introduction

Cell cycle checkpoint (cyclin-CDK complexes) and DNA damage checkpoint (which depend on p53) regulate proper cell division. Inappropriate cell division or loss of normal cellular checks may lead to cancer. Cancer is defined as an uncontrolled growth of abnormal cells. Generally, oncogenes and tumor suppressor genes promote and inhibit the growth of cancer, respectively.

Explanation of Solution

Oncogenes: Oncogenes can cause cancer. They may be mutated or highly expressed in a cell. They can promote uncontrolled cell division, for example, Rous sarcoma virus. The gene of Rous sarcoma virus encodes highly expressive protein kinase, which is similar to signaling protein kinases. This viral gene is called v-src. Oncogenes inhibit the process of apoptosis (a programmed cell death), thereby, they promote survival and continuous proliferation of cancer cells.

Proto-oncogenes: They are normal genes involved in various cellular mechanisms such as cell division and growth. Genetic alteration on the proto-oncogenes due to mutation may lead to the conversion of proto-oncogenes to oncogenes. Nearly most of the proteins involved in the signaling cascade of cell division are products of proto-oncogenes, including growth factors, G-proteins, protein kinases, and cell-surface receptors. Mutation of these genes can result in oncogenes. Proto-oncogenes do not cause cancer directly, however, mutations of proto-oncogenes may induce cancer.

Tumor suppressor genes: Tumor suppressor genes generally inhibit cell division, thereby, they prevent the progression of cancer. They control the uncontrolled cell proliferation, some tumor suppressor genes are involved in checkpoints of the cell cycle, for example, p53.  Other tumor suppressor genes can inhibit the expression of genes that induce cell division. These genes act against proto-oncogenes, therefore, cell division depends on the expression of proto-oncogenes or oncogenes and cell-cycle arrest depends on tumor suppressor genes.