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Review
. 2015:2015:417281.
doi: 10.1155/2015/417281. Epub 2015 Sep 27.

Cancer Microenvironment and Endoplasmic Reticulum Stress Response

Claudia Giampietri  1 , Simonetta Petrungaro  1 , Silvia Conti  1 , Antonio Facchiano  2 , Antonio Filippini  1 , Elio Ziparo  1
Affiliations
Review

Cancer Microenvironment and Endoplasmic Reticulum Stress Response

Claudia Giampietri et al. Mediators Inflamm. 2015.

Abstract

Different stressful conditions such as hypoxia, nutrient deprivation, pH changes, or reduced vascularization, potentially able to act as growth-limiting factors for tumor cells, activate the unfolded protein response (UPR). UPR is therefore involved in tumor growth and adaptation to severe environments and is generally cytoprotective in cancer. The present review describes the molecular mechanisms underlying UPR and able to promote survival and proliferation in cancer. The critical role of UPR activation in tumor growth promotion is discussed in detail for a few paradigmatic tumors such as prostate cancer and melanoma.

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Figures

Figure 1
Figure 1
As a consequence of ER stress cells activate signal transduction pathways collectively known as unfolded protein response (UPR). The figure represents the three branches of the UPR and the corresponding UPR sensors (PERK, IRE1, and ATF6).
Figure 2
Figure 2
Tumor microenvironment factors activate ER stress and UPR responses leading to cancer development and metastases.
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