scholarly journals Mycobacterium Tuberculosis Heat Shock Proteins Use Diverse Toll-like Receptor Pathways to Activate Pro-inflammatory Signals

2005 ◽  
Vol 280 (22) ◽  
pp. 20961-20967 ◽  
Author(s):  
Yonca Bulut ◽  
Kathrin S. Michelsen ◽  
Linda Hayrapetian ◽  
Yoshikazu Naiki ◽  
Ralf Spallek ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Toll Like Receptor ◽  
Inflammatory Signals ◽  
Shock Proteins

scholarly journals Single-cell analysis of basal cell carcinoma reveals heat shock proteins promote tumor growth in response to WNT5A-mediated inflammatory signals

2021 ◽  
Author(s):  
Christian Guerrero-Juarez ◽  
Gun Lee ◽  
Yingzi Liu ◽  
Shuxiong Wang ◽  
Yutong Sha ◽  
...  
Keyword(s):  
Heat Shock ◽  
Tumor Microenvironment ◽  
Basal Cell Carcinoma ◽  
Heat Shock Proteins ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Basal Cell ◽  
Tissue Type ◽  
Inflammatory Signals ◽  
Shock Proteins

How basal cell carcinoma (BCC) interacts with its tumor microenvironment to promote growth is unclear. Here we use singe-cell RNA sequencing to define the human BCC ecosystem and discriminate between normal and malignant epithelial cells. We identify spatial biomarkers of both tumors and their surrounding stroma that reinforce the heterogeneity of each tissue type. Combining pseudotime, RNA velocity, cellular entropy, and regulon analysis in stromal cells reveal a cancer-specific rewiring of fibroblasts where STAT1, TGFbeta, and inflammatory signals induce a non-canonical WNT5A program that maintains the stromal inflammatory state. Cell-cell communication modeling suggests that tumors respond to the sudden burst of fibroblast-specific inflammatory signaling pathways by producing heat shock proteins, which we validated in situ. Finally, dose-dependent treatment with an HSP70 inhibitor suppresses in vitro BCC cell growth and Hedgehog signaling and in vivo tumor growth in a BCC mouse model, validating HSP70s essential role in tumor growth and reinforcing the critical nature of tumor microenvironment crosstalk in BCC progression.

Overexpression of heat-shock proteins reduces survival of Mycobacterium tuberculosis in the chronic phase of infection

10.1038/89113 ◽  
2001 ◽  
Vol 7 (6) ◽  
pp. 732-737 ◽  
Author(s):  
Graham R. Stewart ◽  
Valerie A. Snewin ◽  
Gerhard Walzl ◽  
Tracy Hussell ◽  
Peter Tormay ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Chronic Phase ◽  
Shock Proteins
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