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A tumor suppressor gene (TSG), or anti-oncogene, is a gene that regulates a cell during cell division and replication. [1] If the cell grows uncontrollably, it will result in cancer . When a tumor suppressor gene is mutated, it results in a loss or reduction in its function.
Oncogenomics is a sub-field of genomics that characterizes cancer-associated genes.It focuses on genomic, epigenomic and transcript alterations in cancer. Cancer is a genetic disease caused by accumulation of DNA mutations and epigenetic alterations leading to unrestrained cell proliferation and neoplasm formation.
It was later found that carcinogenesis (the development of cancer) depended both on the mutation of proto-oncogenes (genes that stimulate cell proliferation) and on the inactivation of tumor suppressor genes, that keep proliferation in check. Knudson's hypothesis refers specifically, however, to the heterozygosity of tumor suppressor genes.
DNA oncoviruses typically impair two families of tumor suppressor proteins: tumor proteins p53 and the retinoblastoma proteins (Rb). It is evolutionarily advantageous for viruses to inactivate p53 because p53 can trigger cell cycle arrest or apoptosis in infected cells when the virus attempts to replicate its DNA. [13]
A proto-oncogene is a normal gene that could become an oncogene due to mutations or increased expression. Proto-oncogenes code for proteins that help to regulate the cell growth and differentiation. Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through their protein products.
Tumor suppressor genes are genes that inhibit cell division, survival, or other properties of cancer cells. Tumor suppressor genes are often disabled by cancer-promoting genetic changes. Finally Oncovirinae, viruses that contain an oncogene, are categorized as oncogenic because they trigger the growth of tumorous tissues in the host.
[34] [35] Let-7 and miR15/16 play important roles in down-regulating RAS and BCL2 oncogenes, and their silencing occurs in cancer cells. [18] Decreased expression of miR-125b1, a miRNA that functions as a tumor suppressor, was observed in prostate, ovarian, breast and glial cell cancers.
The transforming activity of TAg is due in large part to its perturbation of the retinoblastoma [1] and p53 tumor suppressor proteins. [2] In addition, TAg binds to several other cellular factors, including the transcriptional co-activators p300 and CBP, which may contribute to its transformation function. [3]