ER stress drives Lipocalin 2 upregulation in prostate cancer cells in an NF-κB-dependent manner.

ABSTRACT:

Background

Tumor cells adapt to endoplasmic reticulum (ER) stress through a set of conserved intracellular pathways, as part of a process termed the unfolded protein response (UPR). The expression of UPR genes/proteins correlates with increasing progression and poor clinical outcome of several tumor types, including prostate cancer. UPR signaling can activate NF-κB, a master regulator of transcription of pro-inflammatory, tumorigenic cytokines. Previous studies have shown that Lipocalin 2 (Lcn2) is upregulated in several epithelial cancers, including prostate cancer, and recently Lcn2 was implicated as a key mediator of breast cancer progression. Here, we hypothesize that the tumor cell UPR regulates Lcn2 production.

Methods

We interrogated Lcn2 regulation in murine and huma

SUBMITTER: Mahadevan NR 

PROVIDER: S-EPMC3146445 | biostudies-literature | 2011 Jun

REPOSITORIES: biostudies-literature