title: Endoplasmic reticulum stress, genome damage, and cancer.
abstract: Endoplasmic reticulum (ER) stress has been linked to many diseases, including cancer. A large body of work has focused on the activation of the ER stress response in cancer cells to facilitate their survival and tumor growth; however, there are some studies suggesting that the ER stress response can also mitigate cancer progression. Despite these contradictions, it is clear that the ER stress response is closely associated with cancer biology. The ER stress response classically encompasses activation of three separate pathways, which are collectively categorized the unfolded protein response (UPR). The UPR has been extensively studied in various cancers and appears to confer a selective advantage to tumor cells to facilitate their enhanced growth and resistance to anti-cancer agents. It has also been shown that ER stress induces chromatin changes, which can also facilitate cell survival. Chromatin remodeling has been linked with many cancers through repression of tumor suppressor and apoptosis genes. Interplay between the classic UPR and genome damage repair mechanisms may have important implications in the transformation process of normal cells into cancer cells.
authors.affiliation: Department of Animal Science, McGill University , Montréal, QC , Canada.
authors.forename: Naomi
authors.initials: N
authors.lastname: Dicks
authors.affiliation: Department of Animal Science, McGill University , Montréal, QC , Canada.
authors.forename: Karina
authors.initials: K
authors.lastname: Gutierrez
authors.affiliation: Department of Biochemistry, University of Alberta , Edmonton, AB , Canada.
authors.forename: Marek
authors.initials: M
authors.lastname: Michalak
authors.affiliation: Department of Animal Science, McGill University , Montréal, QC , Canada.
authors.forename: Vilceu
authors.initials: V
authors.lastname: Bordignon
authors.affiliation: School of Dietetics and Human Nutrition, McGill University , Montréal, QC , Canada.
authors.forename: Luis B
authors.initials: LB
authors.lastname: Agellon
keywords: DNA breaks; carcinogenesis; cell death; chromatin damage; coping responses; endoplasmic reticulum; unfolded proteins