Mitogens act primarily by influencing a set of proteins which are involved in the restriction of progression through the cell cycle.
It, combined with the Ras pathway, downregulate cyclin D1, a cyclin-dependent kinase, if they are not stimulated by the presence of mitogens.
Endogenous mitogens function to control cell division is a normal and necessary part of the life cycle of multicellular organisms.
For example, consider one of the earliest oncogenes to be identified, p28sis from the simian sarcoma virus, which causes tumorigenesis in the host animal.
Scientists found that p28sis has a nearly identical amino acid sequence as human platelet-derived growth factor (PDGF).
Overexpression of HER2 is common in 15-30% of breast cancers,[7] allowing the cell cycle to progress even with extremely low concentrations of EGF.
In other cases, tumor cells possess loss-of-function mutations in some part of the anti-mitogenic pathway.
TGF-𝝱 works by binding to cell-surface receptors and activating the Smad gene regulatory proteins.
Smad proteins then trigger an increase in p15, which inhibits cyclin D1 and prevents cell cycle progression.
Generally, multiple mutations in different subsystems (an oncogene and a tumor suppressor gene) are the most effective at causing cancer.
For example, a mutation that hyperactivates the oncogene Ras and another that inactivates the tumor suppressor pRb is far more tumorigenic than either protein alone.
In tumor cells, there is generally another mutation that inhibits apoptotic proteins as well, suppressing the hyperproliferation stress response.
T cells undergo mitosis when stimulated by mitogens to produce small lymphocytes that are then responsible for the production of lymphokines, which are substances that modify the host organism to improve its immunity.
The most commonly used mitogens in clinical laboratory medicine are: Lipopolysaccharide toxin from gram-negative bacteria is thymus-independent.