Treating a Dysregulated JAK/STAT Pathway in Cancer Cells


  • Jarod M. Schieler Judson University
  • Jeffrey O. Henderson Judson University
Keywords: Cancer, CRISPR/Cas9, Cytokine, JAK/STAT, PIAS, PTPS, SOCS

Abstract


The JAK/STAT pathway is induced by the binding of a cytokine to its cognate receptor. The receptor’s engagement with the cytokine recruits a JAK protein, which activates itself via auto/trans-phosphorylation. In turn, the activated JAKs recruit and phosphorylate STAT proteins. The phosphorylated STAT proteins form a dimer, translocate to the cell nucleus and acts as a transcription factor to induce gene expression. In this way, the JAK/STAT pathway can mediate a cell’s response to extracellular signals. The proteins ultimately induced by the JAK/STAT pathway contribute to processes such as inflammatory response, differentiation, proliferation, and apoptosis. When the JAK/STAT pathway becomes dysregulated, proto-oncogenes and/or tumor-suppressor genes are often inappropriately expressed, commonly resulting in oncogenesis. This review discusses how SOCS, PIAS, and PTPS proteins modulate the JAK/STAT pathway ensuring that it remains cyclic and transient.  The use of jakibins, STAT inhibitors, decoy oligonucleotides, RNA interference and genome editing to synthetically regulate a dysregulated JAK/STAT pathway in cancer cells are also considered.

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Author Biographies

Jarod M. Schieler, Judson University

Biochemistry Major in the Honors Program, Class of 2016

Jeffrey O. Henderson, Judson University

Professor of Biology

Department of Science and Mathematics

 


Published
04-14-2016

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How to Cite
Schieler, J. M., & Henderson, J. O. (2016). Treating a Dysregulated JAK/STAT Pathway in Cancer Cells. Journal of Student Research, 5(1), 11-17. Retrieved from https://jofsr.org/index.php/path/article/view/282
Section
Review Articles