Tissue and Age Specific Expression of the Myc Proto-oncogene Family Throughout the Life Span of the C57BL/6J Mouse Strain
Overview
Authors
Affiliations
The expression of the proto-oncogene myc family (c, L and N) in terms of steady-state mRNA levels was determined in seven different normal non-cancerous tissues throughout the life span (seven different ages) of the C57BL/6J male mouse strain. C-myc oncogene expression was highest in prenatal and newborn ages and then decreased to its lowest levels at about 6 months of age. With further increase of age, a progressive pattern of increase in expression of c-myc was found in brain, liver, skin, and small intestine. However, for kidney, spleen and heart, little or no significant change was evident. Significant differential expression of c-myc was found in most tissues in animals of the same age, with highest expression consistently being found in spleen and liver at all ages. For the N-myc and L-myc oncogenes, expression was also highest in prenatal and newborn tissue as compared to the 6-month young adult, but little or no further change was found at older ages. However, substantial tissue-dependent differences in expression were also found, and no expression at all was detected at any age for N-myc in liver and for L-myc in heart, small intestine and liver. Taken together, these results indicate that the expression of the proto-oncogenes c-, L- and N-myc is dependent not only on tissue and embryonic development, as previously shown by other workers, but also on age past the young adult stage of life span. The age-dependent increase in expression of c-myc oncogene found in normal-appearing non-cancerous tissues is of particular interest as possibly reflecting tissue alterations related to both the aging process and the age-dependent increase in cancer incidence.
MYC-an emerging player in mitochondrial diseases.
Purhonen J, Klefstrom J, Kallijarvi J Front Cell Dev Biol. 2023; 11:1257651.
PMID: 37731815 PMC: 10507175. DOI: 10.3389/fcell.2023.1257651.
Defective bone repletion in aged Balb/cBy mice was caused by impaired osteoblastic differentiation.
Sheng M, Lau K, Rundle C, Alsunna A, Wilson S, Baylink D J Bone Miner Metab. 2022; 40(6):900-913.
PMID: 35947191 PMC: 9722502. DOI: 10.1007/s00774-022-01361-3.
Rutledge E, Lindstrom N, Michos O, McMahon A Dev Biol. 2019; 458(2):164-176.
PMID: 31734175 PMC: 6995766. DOI: 10.1016/j.ydbio.2019.11.007.
Oxidative stress response and Nrf2 signaling in aging.
Zhang H, Davies K, Forman H Free Radic Biol Med. 2015; 88(Pt B):314-336.
PMID: 26066302 PMC: 4628850. DOI: 10.1016/j.freeradbiomed.2015.05.036.
The retrograde response: a conserved compensatory reaction to damage from within and from without.
Jazwinski S Prog Mol Biol Transl Sci. 2014; 127:133-54.
PMID: 25149216 PMC: 4271643. DOI: 10.1016/B978-0-12-394625-6.00005-2.