Journal
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
Volume 703, Issue -, Pages -Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2021.108847
Keywords
IL-1?; SIRT1; c-Jun; Proinflammatory cytokines; Human colon cancer HCT-116 cells
Categories
Funding
- Global Core Research Center (GCRC) [2011-0030001]
- BK21 FOUR Program from the National Research Foundation, Republic of Korea [5120200513755]
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IL-1β-induced upregulation of SIRT1 stimulates the production of proinflammatory cytokines via nuclear accumulation of c-Jun, leading to the growth and progression of colon cancer.
SIRT1 is a mammalian NAD+-dependent deacetylase, which is known to be involved in various physiological events, such as adaptive response to environmental stresses including caloric restriction, as well as in aging and cellular senescence. However, recent studies have revealed overexpression of SIRT1 in many different types of human malignancies, particularly colon cancer. Interleukin-1? (IL-1?) is a proinflammatory cytokine that plays a major role in invasiveness, stemness and progression of colon cancer. However, the interaction between IL-1? and SIRT1 in the tumor development and progression remains elusive. In this study, we found that IL-1? induces SIRT1 protein expression in human colon cancer HCT-116 cells. IL-1?-induced SIRT1 upregulation led to enhanced expression of mRNA transcripts of pro-inflammatory cytokines, IL-6 and IL-8 as well as that of IL-1?. Knockdown of SIRT1 prevented IL-1?-induced phosphorylation and nuclear accumulation of c-Jun. Furthermore, pharmacologic inhibition of SIRT1 abrogated clonogenicity and migrative capability of human colon cancer cells stimulated with IL-1?. In summary, IL-1?-induced SIRT1 upregulation stimulates production of proinflammatory cytokines via a nuclear accumulation of c-Jun, leadng to colon cancer growth and progression.
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