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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.
[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.
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.
If, through mutation, normal genes promoting cellular growth are up-regulated (gain-of-function mutation), they predispose the cell to cancer and are termed oncogenes. Usually, multiple oncogenes, along with mutated apoptotic or tumor suppressor genes, act in concert to cause cancer. Since the 1970s, dozens of oncogenes have been identified in ...
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.
This is a step toward tumor progression. [2] [3] In order for a tumor cell to survive, it must decrease its expression of tumor suppressor genes such as p53, BRCA1, BRCA2, RB1, or the fas receptor. [4] [5] A tumor suppressor would trigger an apoptotic pathway in a cancer cell if there were DNA damage, polyploidy, or uncontrolled cell growth.
Role of tumor suppressor and oncogenes [ edit ] Apart from being as a general tumor suppressor gene , p53 also plays an important part in regulating of metabolism. p53 activates hexokinase 2 (HK2) that converts glucose to glucose-6-phosphate (G6P) which enters glycolysis to produce ATP, or enters the pentose phosphate pathway (PPP) .
The classical view of cancer is a set of diseases driven by progressive genetic abnormalities that include mutations in tumor-suppressor genes and oncogenes, and in chromosomal abnormalities. A role for epigenetic alterations was identified in the early 21st century. [100]