Cell carcinogenesis is related to the "self-destructive protein"

Russian researchers have recently discovered a mechanism behind cell carcinogenesis: under normal circumstances, the programmed cell death mechanism will cause cells with signs of cancer to die, but if the signal molecule protein that causes cancer cells to self-destruct is not found on the surface of the cell membrane If you reach a foothold, you will not be able to suppress the progression of cancer.

Researchers have discovered that cervical cancer cells, a signal molecule called "fasl protein", can penetrate cells with signs of cancer, trigger an immune response, and cause "problem cells" to program death. To study the mechanism, the research team developed a human cervical cancer cell line to observe the interaction between fasl protein and cervical cancer cells.

The results showed that there were many “hole-like invagination” structures on the outer surface of cervical cancer cells, and the receptor protein, caveolin-1, was distributed in the “pit”. The C-region and the N-region of the protein end each have a site that binds to the fasl protein, thereby leading the latter through the cell membrane, causing the cancer cells to self-destruct. However, if the two binding sites of caveolin-1 are all missing, it will cause the fasl protein to have nowhere to stay on the outer surface of the cervical cancer cell membrane, and it is even more impossible to "pass through the wall", thus failing to trigger cancer cells. destroy.

Based on this clue, the team found that other signaling proteins responsible for triggering cell self-destruction could not accomplish their mission because of the lack of binding sites for their paired receptor proteins.

Moscow State University researcher Gogwaze said that in the next stage he and his colleagues will further study the "hands-on" nature of fasl protein and caveolin-1 and other protein partners, in order to find a way to trigger cell self-destruction of signal molecules Forced into cancerous target cells to prevent other healthy cells from becoming cancerous.

The research results were published by experts from the Moscow State University and the Institute of Theoretical and Experimental Biophysics of the Russian Academy of Sciences in the journal "Cell Death and Disease", a journal of Nature. (Xinhua)

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