Molecular Switch of AhR in Repression or Activation of Stem Cell Signaling

Title:Molecular Switch of AhR in Repression or Activation of Stem Cell Signaling

Volume: 12 Issue: 1

Author(s): Yingqiu Xie*, Xiuqing Zhang, Tomiris Atazhanova, Bindong Song and Qing Yang

Affiliation:

• Department of Biology, School of Science and Technology, Nazarbayev University, Astana 010000,Kazakhstan

Keywords: AhR, cancer, stem cell, OCT4, TCDD, molecular switch.

Abstract: Background: Aryl hydrocarbon receptor (AhR) is an exogenous ligand-activating or constitutively active transcription factor. AhR regulates cellular differentiation, cell migration and other molecular and cellular processes. In general, AhR is biologically a very complex molecule in terms of its structure and functions in stemness, differentiation and clinical diseases. Here we review the debated issue of AhR in stem cell and cancer stem cell signaling.

Methods: We searched literatures in PubMed and Google Scholar for related articles to review the AhR function and signal transduction in stem cells and cancer stem cells. Experimental data and results were analyzed.

Results: It has been shown that AhR is an oncogenic protein but recent studies suggest that AhR can also inhibit cancer signaling through cancer stem cell pathways which are mostly common in OCT4. AhR either activates or inhibits tumorigenesis possibly through regulation of stemness or differentiation. Furthermore, how AhR can switch this function is largely unknown.

Conclusion: AhR may inhibit or promote stem cell/cancer stem cell signaling through molecular switches of ageing, tissue specific signaling, ligand, and systems interaction networks. Targeting these signaling would provide a new avenue for efficient therapy in precision medicine.

Cite this article as:

Xie Yingqiu*, Zhang Xiuqing, Atazhanova Tomiris, Song Bindong and Yang Qing, Molecular Switch of AhR in Repression or Activation of Stem Cell Signaling, Current Signal Transduction Therapy 2017; 12 (1) . https://dx.doi.org/10.2174/1574362412666170207103318

DOI https://dx.doi.org/10.2174/1574362412666170207103318	Print ISSN 1574-3624
Publisher Name Bentham Science Publisher	Online ISSN 2212-389X