Metabolism and epigenetics of pancreatic cancer stem cells

Pancreatic Cancer (PDA) is an aggressive malignancy characterized by early spread and a high mortality. Current studies suggest that a subpopulation of cells exist within tumors, cancer stem cell (CSC), which are capable of self-renewal and give rise to unique progeny which form the major neoplastic...

Full description

Saved in:
Bibliographic Details
Published in:Seminars in cancer biology 2019-08, Vol.57, p.19-26
Main Authors: Perusina Lanfranca, M., Thompson, J.K., Bednar, F., Halbrook, C., Lyssiotis, C., Levi, B., Frankel, T.L.
Format: Article
Language:English
Subjects:
Acinar-ductal-metaplasia
Animals
Cancer stem cells
Carcinoma, Pancreatic Ductal - genetics
Carcinoma, Pancreatic Ductal - metabolism
Carcinoma, Pancreatic Ductal - pathology
Cell Plasticity
Disease Susceptibility
Energy Metabolism
Epigenesis, Genetic
Epigenetics
Epithelial-Mesenchymal Transition
Epithelial-to-mesenchymal transition
Gene Expression Regulation, Neoplastic
Humans
Metabolism
Neoplastic Stem Cells - metabolism
Neoplastic Stem Cells - pathology
Pancreatic cancer
Pancreatic Neoplasms - genetics
Pancreatic Neoplasms - metabolism
Pancreatic Neoplasms - pathology
Stemness
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Pancreatic Cancer (PDA) is an aggressive malignancy characterized by early spread and a high mortality. Current studies suggest that a subpopulation of cells exist within tumors, cancer stem cell (CSC), which are capable of self-renewal and give rise to unique progeny which form the major neoplastic cellular component of tumors. While CSCs constitute a small cellular subpopulation within the tumor, their resistance to chemotherapy and radiation make them an important therapeutic target for eradication. Along with distinctive phenotypic properties, CSCs possess a unique metabolic plasticity allowing them to rapidly respond and adapt to environmental changes. These cells and their progeny also display a significantly altered epigenetic state with distinctive patterns of DNA methylation. Several mechanisms of cross-talk between epigenetic and metabolic pathways in PDA exist which ultimately contribute to the observed cellular plasticity and enhanced tumorigenesis. In this review we discuss various examples of this metabolic-epigenetic interplay and how it may constitute a new avenue for therapy specifically targeting CSCs in PDA.
ISSN:1044-579X
1096-3650
DOI:10.1016/j.semcancer.2018.09.008