SCIENTIFIC RESEARCH shows that a protein commonly activated in cancer cells drives systemic stress-driving functions of tumor cells — also known as myosin light-sensing nuclear factor 4-cogene. This raises the possibility that targeting this protein may help reverse cancer-associated cellular stress and improve therapies for various types of cancer says Michael Bourque Ph. D. a professor of Pharmacology at the University of Montreal Hospital Research Center and lead of the research team on the study.
The findings are published on 365 days after the publication of the journal Cell Reports. The appearance of this unique feature in cancer cells that have adapted to chronic stress likely due to their ability to evade immune-mediated destruction is very encouraging — since one of the aims of the authors research is to look at cell senescence the aging process which is also mediated by myosin light-sensing nuclear factor 4-cogene levels.
We were very excited about this says Bourque who detailed the findings in an article entitled Identifying stress responsive factors in cancer through myosin light-sensing nuclear factor- a systematic analysis of cancer-associated homeostasis with epidemiologic and clinical data.
Cancer cells are known to be susceptible to chronic stress due to the uncontrolled growth (mitotic) invasion (metastosis) and metastasis (progression). It is known that acute and chronic stress drive proliferation says Bourque. Our new findings raise the possibility that in addition to chronic non-healing stress response cancer cells are also vulnerable to acute adaptive andor adaptive stress responses which could point towards novel therapeutic approaches.
All cells undergo some degree of cell senescence at some time in their evolution. Cell aging in which tumors stop dividing (autophagy) leads to a loss of some cells due to a depletion of sugars and of cellular fats. This is particularly true for cancer cells which over time lose large amounts of parabiotic-associated fibroblasts (a common cell type). Understanding current cellular strategies to compensate for this loss and promote cell survival is crucial for enhancing the impact of cancer therapeutics.