Death cancer cells can make living glioma cells more resistant.

Highlights of this study: apoptocytic extravehicular vesys (apoEVs) can promote the production of more malignant, more treatable neuroglioma (glioblastoma, GBM);
the proliferation of tumor cells in malignant tumors like GBM is mixed with many apoptosis cells, but researchers have not previously noticed the intercellular signaling exchange between these apoptosis cells and living cells. in a recent study published in Cancer Cell,
, researchers at the University of Alabama at Birmingham found that apoptotic GBM cells can promote the continued proliferation of viable GBM cells and improve their tolerance to treatment by secreting apoEVs rich in different shear components.
apoEVs alters the RNA splicing of receptor GBM cells, thus facilitating the transition of these cells to more resistant, malignant, and easier-to-migrate phenotypes.
through mechanism research, the researchers found that RBM11 is a representative splicing factor that is significantly raised after tumor treatment, and once the tumor cell apoptosis occurs it will be enriched in apoEVs.
once these apoEVs are swallowed by the receptor GBM cells, these exogenous RBM11 slicing states alter MDM4 and the cell cycle protein D1, allowing them to express more carcinogenic forms of protein, making these GBM cells more resistant to treatment and more malignant.
in general, the study found that apoptosis GBM cells also play their "residual heat" to help the remaining GBM cells escape the lethality of the treatment, and suppressing these apoEVs may be a new way to prevent drug resistance and tumor recurrence.
.