Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Nov 27;14:1245421. doi: 10.3389/fimmu.2023.1245421

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2023 Guha, Goswami, Sultana, Ganguly, Choudhury, Chakravarti, Bhuniya, Sarkar, Bera, Dhar, Das, Das, Baral, Bose and Banerjee

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

The interaction between MDSCs and BCSCs. Representative image of the interaction between MDSCs and BCSCs. MDSCs are recruited to the tumor site by ΔNp63-dependent activation of chemokines CXCL2 and CCL22. They secrete pro-metastatic factors such as MMP9 and chitinase 3-like 1 to induce BCSC enrichment. MDSCs cause IL-6-dependent phosphorylation of STAT3 that promotes NOTCH signaling (NOTCH2, NOTCH3, HEY1, HEY2, and CHERP transcripts and the intracellular domain of NOTCH) expression through nitric oxide (NO), leading to persistent STAT3 activation that results in the induction of EMT with high expression genes like Vimentin, CK14, and TWIST.