What is induced cellular senescence?
In response to cellular stress or damage, proliferating cells can induce a specific program that initiates a state of long-term cell-cycle arrest, termed cellular senescence. Accumulation of senescent cells occurs with organismal aging and through continual culturing in vitro.
How is cellular senescence related to cancer?
Senescence is a double-edged sword that can function in opposite directions. It is a potential mechanism for a cell to avoid malignant transformation. However, senescence can also promote cancer development by altering the cellular microenvironment through a senescence-associated secretory phenotype (SASP).
What happens cellular senescence?
The senescence response causes striking changes in cellular phenotype. These changes include an essentially permanent arrest of cell proliferation, development of resistance to apoptosis (in some cells), and an altered pattern of gene expression.
What is cellular senescence explain the mechanism?
Figure 2. Schematic of the different mechanisms involved in Senescence Associated Secretory Phenotype (SASP) regulation. This figure shows the different pathways involved in regulating SASP. Most of the pathways converge to activate the transcription factors NF-κB and c/EBPβ in senescent cells.
What is therapy induced senescence?
Therapy-induced cellular senescence is a state of stable growth arrest induced by common cancer treatments such as chemotherapy and radiation. In an oncogenic context, therapy-induced senescence can have different consequences.
What senescence mean?
The process of growing old. In biology, senescence is a process by which a cell ages and permanently stops dividing but does not die. Over time, large numbers of old (or senescent) cells can build up in tissues throughout the body.
How do you induce senescence in cells?
Various oxidative stresses have been used to induce premature senescence, including exposure to hydrogen peroxide (26), ultraviolet (UV) light (27), tert-butylhydroperoxide (28), and hyperoxia (18), among which hydrogen peroxide is the most commonly used inducer.
What is oncogene mutations?
An oncogene is a mutated gene that contributes to the development of a cancer. In their normal, unmutated state, onocgenes are called proto-oncogenes, and they play roles in the regulation of cell division. Some oncogenes work like putting your foot down on the accelerator of a car, pushing a cell to divide.
What is the oncogene theory?
In the mid-1970s, the American microbiologists John Michael Bishop and Harold Varmus tested the theory that healthy body cells contain dormant viral oncogenes that, when triggered, cause cancer. They showed that oncogenes are actually derived from normal genes (proto-oncogenes) present in the body cells of their host.
What is oncogene-induced cellular senescence ( OIS )?
Oncogene-induced cellular senescence (OIS) is a complex program that is triggered in response to aberrant activation of oncogenic signaling. Initially, OIS was thought to be a barrier to malignant transformation because of its suppression on cell proliferation.
How does the induction of p16 affect senescence?
Senescent cells are often accompanied by the induction of p16, which affects the maintenance of cellular senescence. Cells expressing low levels of p16 would circumvent senescence and resume proliferation 9. RB exists downstream of p16 and plays a crucial role in cellular senescence.
How is autophagy related to the acquisition of senescence?
A subset of autophagy-related genes is up-regulated during senescence. The overexpression of ULK3 induced autophagy and senescence, while the inhibition of autophagy delayed the OIS-related phenotype, including senescence-associated secretion, suggesting that autophagy and its effectors mediated the acquisition of the senescence phenotype 35.