publication . Article . 2010

Differential interleukin-6/Stat3 signaling as a function of cellular context mediates Ras-induced transformation

Katrina Podsypanina; Kenneth Leslie; Hao Ho; Lionel B. Ivashkiv; Marjan Berishaj; Jacqueline Bromberg; Sizhi P. Gao;
Open Access English
  • Published: 01 Oct 2010 Journal: Breast Cancer Research, volume 12, issue 5 (issn: 1465-542X, Copyright policy)
  • Publisher: Springer Nature
Abstract
Introduction Tyrosine phosphorylated signal transducer and activator of transcription 3 (pStat3) is expressed in numerous cancers and is required for mediating tumorigenesis. Autocrine and paracrine interleukin (IL)-6 signaling is the principal mechanism by which Stat3 is persistently phosphorylated in epithelial tumors including breast, lung, colon and gastric cancer. The Ras oncogene mediates cellular transformation without evidence of pStat3 in cultured cells. However, non-tyrosine phosphorylated Stat3 was shown to function as a transcriptional activator, localize to the mitochondria and regulate ATP synthesis and mediate cell migration. Here we examined the ...
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doi: 10.1186/bcr2725
pmc: PMC3096973
pmid: 20929542
Subjects
free text keywords: Medicine(all), Cancer Research, Oncology, Research Article, Oncogene, STAT3 Transcription Factor, Paracrine signalling, Autocrine signalling, STAT3, biology.protein, biology, Interleukin, Signal transduction, STAT protein, Cell biology
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NIH| Role of Stat3 in Breast Cancer Tumorigenesis
Project
Role of Stat3 in Breast Cancer Tumorigenesis
  • Funder: National Institutes of Health (NIH)
  • Project Code: 5R01CA087637-03
  • Funding stream: NATIONAL CANCER INSTITUTE
, NIH| MOUSE GENETICS
Project
MOUSE GENETICS
  • Funder: National Institutes of Health (NIH)
  • Project Code: 2P30CA008748-43
  • Funding stream: NATIONAL CANCER INSTITUTE
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