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Editorial Volume 4 Issue 2
Prion: a janus-faced protein in cancer
Erdal Balcan
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Department of Biology, Manisa Celal Bayar University, Turkey
Correspondence: Erdal Balcan, Department of Biology, Faculty of Arts and Science, Molecular Biology Section, Manisa Celal Bayar University, Sehit Prof. Dr. Ilhan Varank Campus 45047 Manisa, Turkey
Received: October 26, 2017 | Published: October 30, 2017
Citation: Balcan E. Prion: a janus-faced protein in cancer. J Appl Biotechnol Bioeng. 2017;4(2):547. DOI: 10.15406/jabb.2017.04.00097
Editorial
Prion is a key protein in the pathogenesis of neurodegenerative diseases so called transmissible spongiform encephalopathies (TSEs) and in cancer. The name of “prion” evolved from “Proteinaceous Infectious particle” which refers to two conformational isoforms of prion protein, endogenous cellular variant PrPc, and its pathogen, mis-folded and aggregated conformer, PrPSc.1 Under some circumstances, physiological form of protein PrPc can transform to pathogen isoform, PrPSc that is associated with TSEs including fatal familial insomnia, Creutzfeldt-Jakob disease and Kuru in humans. PrPc is a glycophosphatidylinositol-anchored cell surface glycoprotein and can interact with the cytosolic membrane bound organelles and with cytoskeleton. This protein highly accumulated in the central nervous system. However the transcripts of PrPc encoding gene (PRNP) can also be expressed in many other tissues including lymphoid organs. As a cell surface molecule, PrPc has many interaction partners including transmembrane and secreted proteins. It also interact a variety of intracellular proteins. Based on the its potential binding partners, PrPc has been proposed to participate a broad array of cellular events such as cell death and survival, signal transduction, differentiation and cell adhesion.2–5 Due to transformation of PrPc into PrPSc, which leads to misfolding and induces apoptotic machinery thereby neurodegeneration (Gain of function effect), surveying the biological activity of PrPc seems to be critical for understanding the etiology and pathogenesis of prion diseases.6–8
Since the last 20 years, the concepts of cancer biology and cancer genetics have an important place in our life. Although ongoing clinical and laboratory researches have increased the survival rate and the quality of life in cancer patients, many cellular mechanisms still remain largely mysterious in cancer biology. Among these cellular events, programmed cell death types and the genes that control them have a unique significance because they have a profound effect on the malignant phenotype in tumorigenesis as well as in cancer treatment. Multidrug resistance (MDR) of tumor cells, characterized by decreased drug uptake, increased drug efflux and evasion of drug-induced apoptosis, is the major factor in the failure of cancer chemotherapy. Recent studies have indicated that the CD44 and PrPc coordinately increase the MDR phenotype in cancer stem cells by inducing the over expression of cell surface ATP-binding cassette transporters (Pgp-1) and, hence enhance the malignancy.9–11 Several intriguing lines of evidence indicating that PrPc over expression protect tumor cells from Bax-mediated apoptosis and/or autophagy-dependent cell death. Apparently, PrPc has a pivotal role in cancer prognosis as well as in TSE pathogenesis. More importantly, future progress in understanding the function of PrPc, can be effective on the development and implementation of PrPc-targeting novel therapeutic strategies.
Acknowledgements
None.
Conflict of interest
The author declares no conflict of interest.
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©2017 Balcan. This is an open access article distributed under the terms of the, which permits unrestricted use, distribution, and build upon your work non-commercially.