CTOnews.com, Nov. 29 (Xinhua)-- scientists have released a new study that addresses for the first time the debate over how mutated proteins drive tumor growth. This finding not only helps to rethink the treatment of cancer, but also may lead to new and improved treatments.
At present, the academic consensus is that the TP53 gene controls the production of the protein p53, which plays a key role in repairing or destroying the DNA of damaged cells.
P53 is a tumor suppressor that regulates cell division and prevents cells from proliferating too fast or in an uncontrolled way.
P53 mutations are present in more than half of human cancers. These mutations may be triggered by exposure to environmental factors such as ultraviolet radiation, or may be hereditary.
In academic circles, there are contradictory views on whether p53 mutation will cause loss of function or acquisition.
Loss of function means that the protein does not regulate the cellular response that prevents tumor development and growth; function acquisition is a super-strong protein that helps cancer cells survive and proliferate.
Researchers from the Walter and Elizabeth Hall Institute (WEHI) in Australia worked with the University of Trento in Italy to resolve the debate, discovering for the first time which features of the mutated p53 protein are critical to the growth of cancer.
Gemma Kelly, co-author of the study, said:
About 50% of all cancers in humans are accompanied by p53 mutations.
Cancers such as pancreatic cancer, lung cancer and breast cancer are usually due to defects in these proteins, and our findings change our understanding of these mutations, which helps to rethink how to target them in the development of new cancer treatments.
The researchers used CRISPR / Cas9 techniques to genetically inactivate 12 different mutant TP53 genes that produce function and gain activity in human cancer cell lines.
The results showed that the removal of mutant p53 had no effect on the survival or proliferation of the tested cancer cell lines in vitro. It also does not affect the content or activity of mitochondria or the level of intracellular reactive oxygen species (ROS); increased cellular metabolism and intracellular ROS levels are markers of cancer.
Xenotransplantation of human and mouse cancer cell lines and colon cancer-derived organs in immunodeficient mice-considered to be the gold standard model for the study of human tumor growth-shows that the removal of mutant p53 does not damage tumor growth or metastasis. In addition, the normal function of p53 is restored and lost when the protein is mutated, thereby reducing cancer growth in preclinical models.
Our research provides the first evidence that it is actually loss of function that affects the growth of cancer. We found no evidence that functional acquisition led to cancer growth.
CTOnews.com is enclosing the address of the thesis examination: Zilu Wang; Matteo Burigotto; Sabrina Ghetti; Francois Vaillant; Tao Tan; Bianca D. Capaldo; Michelle Palmieri; Yumiko Hirokawa; Lin Tai; Daniel S. Simpson; Catherine Chang; Allan Shuai. Huang; Elizabeth Lieschke; Sarah T. Diepstraten; Deeksha Kaloni; Chris Riffkin; David C.S. Huang; Connie SN. Li Wai Suen; Alexandra L. Garnham; Peter Gibbs; Jane E. Visvader; Oliver M. Sieber; Marco J. Herold; Luca L. Fava; Gemma L. Kelly; Andreas Strasser,Loss-of-function but not gain-of-function properties of mutant TP53 are critical for the proliferation, survival and metastasis of a broad range of cancer cells,OCTOBER 25 2023, https://doi.org/10.1158/2159-8290.CD-23-0402
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