An NFκB-dependent mechanism of tumor cell plasticity and lateral transmission of aggressive features.

ABSTRACT: Breast cancer is a complex disease exhibiting extensive inter- and intra-tumor heterogeneity. Inflammation is a well-known driver of cancer progression, often attributed to immune cells infiltrating the tumor stroma. However, tumor cells themselves are capable to secrete a variety of inflammatory molecules, of which we understand very little about their role in intra-clonal communication. We recently reported the capacity of triple negative cell lines to induce a cancer stem cell (CSC)-like phenotype and invasion properties into luminal cells, a mechanism mediated by pro-inflammatory cytokines that up-regulated the CXCL12/CXCR4/CXCR7 chemokine signaling axis. We performed transcriptional array analyses of CSCs-associated genes and cancer-inflammatory cell crosstalk genes and built regulato

SUBMITTER: Espinoza-Sanchez NA 

PROVIDER: S-EPMC6003573 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature