Journal article
Constitutive STAT3 Serine Phosphorylation Promotes Helicobacter-Mediated Gastric Disease
JJ Balic, MI Saad, R Dawson, AJ West, L McLeod, AC West, K D'Costa, V Deswaerte, A Dev, W Sievert, DJ Gough, PS Bhathal, RL Ferrero, BJ Jenkins
American Journal of Pathology | ELSEVIER SCIENCE INC | Published : 2020
Abstract
Gastric cancer is associated with chronic inflammation (gastritis) triggered by persistent Helicobacter pylori (H. pylori) infection. Elevated tyrosine phosphorylation of the latent transcription factor STAT3 is a feature of gastric cancer, including H. pylori–infected tissues, and aligns with nuclear transcriptional activity. However, the transcriptional role of STAT3 serine phosphorylation, which promotes STAT3-driven mitochondrial activities, is unclear. Here, by coupling serine-phosphorylated (pS)-STAT3–deficient Stat3SA/SA mice with chronic H. felis infection, which mimics human H. pylori infection in mice, we reveal a key role for pS-STAT3 in promoting Helicobacter-induced gastric path..
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Funding Acknowledgements
Supported by a National Health and Medical Research Council (NHMRC) of Australia research grant (B.J.J.), the Operational Infrastructure Support Program by the Victorian Government of Australia, an Australian Postgraduate Awards scholarship from the Australian Government (J.J.B.), a National Health and Medical Research Council (NHMRC) Early Career Fellowship (A.C.W.), an NHMRC Career Development Fellowship and a grant from the United States Department of Defense (D.J.G.), and NHMRC Senior Medical Research Fellowships (B.J.J. and R.L.F).