A Distinct Role for Interleukin‐6 as a Major Mediator of Cellular Adjustment to an Altered Culture Condition. Issue 11 (9th September 2015)

• Record Type: Journal Article
• Authors: Son, Hwa‐Kyung; Park, Iha; Kim, Jue Young; Kim, Do Kyeong; Illeperuma, Rasika P.; Bae, Jung Yoon; Lee, Doo Young; Oh, Eun‐Sang; Jung, Da‐Woon; Williams, Darren R.; Kim, Jin
• Is Part Of: Journal of cellular biochemistry. Volume 116:Issue 11(2015:Nov.)
• Page Start: 2552
• Page End: 2562
• Publication Date: 2015-09-09
• Subjects: Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.25200
• Languages: English
• ISSNs: 0730-2312

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>ABSTRACT</title> <sec id="jcb25200-sec-0001" sec-type="section"> <p>Tissue microenvironment adjusts biological properties of different cells by modulating signaling pathways and cell to cell interactions. This study showed that epithelial–mesenchymal transition (EMT)/ mesenchymal–epithelial transition (MET) can be modulated by altering culture conditions. HPV E6/E7‐transfected immortalized oral keratinocytes (IHOK) cultured in different media displayed reversible EMT/MET accompanied by changes in cell phenotype, proliferation, gene expression at transcriptional, and translational level, and migratory and invasive activities. Cholera toxin, a major supplement to culture medium, was responsible for inducing the morphological and biological changes of IHOK. Cholera toxin per se induced EMT by triggering the secretion of interleukin 6 (IL‐6) from IHOK. We found IL‐6 to be a central molecule that modulates the reversibility of EMT based not only on the mRNA level but also on the level of secretion. Taken together, our results demonstrate that IL‐6, a cytokine whose transcription is activated by alterations in culture conditions, is a key molecule for regulating reversible EMT/MET. This study will contribute to understand one way of cellular adjustment for surviving in unfamiliar conditions. J. Cell. Biochem. 116: 2552–2562, 2015. © 2015 Wiley Periodicals, Inc.</p> </sec> </abstract>