They discover the main mechanism used by lung cancers to evade immune attack
MADRID, Jan 11. (EUROPA PRESS)
Researchers at Weill Cornell Medicine (United States) have discovered, in a study published in the journal ‘Nature Communications’, the main mechanism used by lung cancers to evade immune attack.
Specifically, experts have seen that a protein, often found at high levels in lung cancer cells, controls an important immunosuppressive pathway that allows tumors to evade immune attack.
This discovery could accelerate the development of treatments that overcome this tumor defense mechanism and improve therapeutic results.
To reach this conclusion, the researchers analyzed human lung cancer data sets and conducted experiments in preclinical models of lung cancer to demonstrate that the transcription factor XBP1 improves tumor survival by suppressing the anticancer activity of cells. neighboring immune cells.
Thus, they discovered that XBP1s exert this effect by boosting the production of an immunosuppressive molecule, prostaglandin E2.
We discovered that XBP1 is a component of a crucial pathway in cancer cells that controls the local immune milieu in lung tumors and may be turned off to boost immunity against cancer, the specialists stressed.
When IRE1a is activated in stressed cells, it begins to produce XBP1, a multitasking transcription factor that controls the expression of various genetic programs in a specific context.
The researchers analyzed the expression levels of the gene encoding XBP1 from a large set of human NSCLC samples cataloged in a national database and found evidence that patients whose tumors had higher levels of XBP1 had a worse chance.
The findings suggest that knocking out IRE1a-XBP1 might be a good treatment strategy for NSCLC and that it might work particularly well in combination with other immunotherapy approaches.
Targeting IRE1a-XBP1 could represent a useful dual therapeutic approach that controls lung cancer progression while inducing protective antitumor immunity.
We are now very interested in finding ways to selectively target an IRE1a-blocking drug in tumor cells.