Stress-induced metastasis: The NET effect
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
View abstract on PubMed
Summary
This summary is machine-generated.Chronic stress hormones called glucocorticoids fuel cancer spread by triggering neutrophil extracellular traps (NETs). This research uncovers a key mechanism linking stress to cancer metastasis and microenvironment remodeling.
Area Of Science
- Oncology
- Immunology
- Endocrinology
Background
- Chronic stress is linked to cancer progression and metastasis.
- The precise molecular mechanisms mediating this connection are not fully understood.
Purpose Of The Study
- To investigate how chronic stress influences cancer metastasis.
- To identify the specific pathways through which stress hormones impact tumor spread.
Main Methods
- Analysis of glucocorticoid effects on cancer cells and the tumor microenvironment.
- Investigation of neutrophil extracellular trap (NET) formation in response to stress mediators.
- Assessment of microenvironment remodeling associated with stress-induced metastasis.
Main Results
- Glucocorticoids, released during chronic stress, were found to promote cancer metastasis.
- Stress-induced glucocorticoids facilitate metastasis by inducing the formation of neutrophil extracellular traps (NETs).
- These processes involve significant remodeling of the tumor microenvironment.
Conclusions
- Glucocorticoids play a critical role in mediating the pro-metastatic effects of chronic stress.
- NET formation is a key mechanism by which stress promotes cancer spread.
- Targeting stress pathways or NET formation may offer novel therapeutic strategies for cancer metastasis.
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
Related Concept Videos
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...