There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
Tumour cells endure both oncogenic and environmental stresses during cancer progression.
Transformed cells must meet increased demands for protein and lipid production needed
for rapid proliferation and must adapt to exist in an oxygen- and nutrient-deprived
environment. To overcome such challenges, cancer cells exploit intrinsic adaptive
mechanisms such as the unfolded protein response (UPR). The UPR is a pro-survival
mechanism triggered by accumulation of unfolded or misfolded proteins in the endoplasmic
reticulum (ER), a condition referred to as ER stress. IRE1, PERK and ATF6 are three
ER anchored transmembrane receptors. Upon induction of ER stress, they signal in a
coordinated fashion to re-establish ER homoeostasis, thus aiding cell survival. Over
the past decade, evidence has emerged supporting a role for the UPR in the establishment
and progression of several cancers, including breast cancer, prostate cancer and glioblastoma
multiforme. This review discusses our current knowledge of the UPR during oncogenesis,
tumour growth, metastasis and chemoresistance.