Everything you ever wanted to know about the p53 tumor suppression gene but were afraid to ask!
Tumor Suppression: Targeting p53 pathways: mechanisms, structures, and advances in therapy, notes taken from an abstract,
The TP53 tumor suppressor is the most frequently altered gene in human cancers, and has been a major focus of oncology research…
(it) plays critical roles in regulating cell cycle, apoptosis, and genomic stability, and is widely regarded as the “guardian of the genome”.
p53 also regulates cell metabolism, ferroptosis, tumor microenvironment, autophagy and so on, all of which contribute to tumor suppression. Mutations in TP53 not only impair its tumor suppressor function, but also confer oncogenic properties to p53 mutants. (Tending to cause or give rise to tumors)
An oncogene is a gene that has the potential to cause cancer.[1] In tumor cells, these genes are often mutated, or expressed at high levels.[2]
Most normal cells will undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered and malfunction. Activated oncogenes can cause those cells designated for apoptosis to survive and proliferate instead.[3
Usually, multiple oncogenes, along with mutated apoptotic or tumor suppressor genes, will all act in concert to cause cancer.
The biological function of p53 in cancer
p53 controls a wide range of signaling networks. There is no simple and clear answer to the question of exactly how, when, and what p53 does. Nevertheless, what is clear is that p53 has a very flexible and versatile response, with an integrated response to environmental perturbations determining cell death or maintaining cellular homeostasis. p53 serves as a linkage point for multiple cellular signaling pathways, harmoniously and delicately regulating various biological functions through transcriptional regulation and protein-protein interactions.
p53 is considered as the guardian of the genome. It plays an important role in maintaining genomic stability. When DNA is damaged, p53 protects the genome by coordinating multiple DNA damage response mechanisms.51 The p53 protein activates the expression of DNA repair proteins DDB2 and XPC.52 The interaction of these proteins with effector proteins may lead to various cell fates, such as apoptosis, senescence or tumorigenesis.53,54
Metabolic homeostasis
Tumor cells require large amounts of biological raw materials and energy to achieve their rapid and sustained growth. The Warburg effect,90 which was first proposed, states that tumor cells metabolize glucose differently than normal cells, as evidenced by enhanced glycolysis and increased lactate production.91 p53 regulation of the glycolytic pathway helps maintain the homeostasis of cellular metabolism and thus acts as a tumor suppressor.
This is a youtube about what this is doing for animals https://www.youtube.com/watch?v=aGb_Cv_eIdo
An interview with the biochemist who created it :https://www.youtube.com/watch?v=Wtz2I0bRItk
