A recent study revealed a new role for the gene “XPR1” (XPR1) in promoting ovarian cancer growth using different mechanisms, and the gene has identified a decisive factor that affects the aggression of ovarian cancer through its interaction with specific cellular paths.
These results highlight new treatment targets for ovarian cancer, a malignant tumor known for its misfortune and resistance to immune checkpoint inhibitors, and the checkpoint inhibitors work by preventing cancer cells from sending signals that deceive the immune system and delude it as normal.
The study highlights that the XPR1 expression increases significantly in ovarian cancer tissue compared to natural ovarian tissues. This increased expression is associated with the advanced cancer stages, the decrease in the survival rate in general, and the low survival rate without development.
Subsequent experiments confirmed that the XPR1 was reduced and spreading ovarian cancer cells, while excessive expression led to an opposite effect, indicating its role in promoting cancer growth. The study provides a basis for future research on the use of self -accumulation rates with immune checkpoint inhibitors to improve the results of treatment, and self -accumulation in which the cell dismantles and destroys proteins and other old, damaged or abnormal substances in cytoplasm (liquid inside the cell).
The study was conducted by scientists from the Chongzing University Medical University in China, and its results were published in the Genes & Diseases Journal on June 24, and the Yurrick Alert website was written about.
One goal in different ways
Other analyzes have revealed that XPR1 interacts with the LEMP1 protein, a major membrane protein associated with legosom, and regulates its expression.
This reaction adjusts self -accumulation, especially during the early stage of it, and the XPR1 silence increased the formation of lyzosome and self -accumulation, while excessive expression led to the suppression of these processes, and lesusome are alectrings surrounded by a membrane that contains a group of enzymes capable of breaking all types of biological polymers: proteins, DNA, carbohydrates, and fats.
In addition to organizing self -accumulation, the study determined a decisive role for XR1 in immunosuppressive evasion. It was found that the complicated particles of the main textile compatibility of the first class (MHC-I), which are proteins found on the surfaces of the cells, are organized by XPR1 through self-devotion.
The XPR1, with the use of chlorokin, a self -devoured inhibitor, enhances the presence of steroids steroids on ovarian cancer cells significantly, which helps the deadly T cells to identify and kill them.
This compound treatment reduces the growth of the tumor in mice models, indicating that targeting XPR1 along with self -devotion can improve the effectiveness of immunotherapy in ovarian cancer.