Scientists have explained how cancer "zombie cells" come to life

 Mutating cells can prevent cancer from spreading by putting themselves into a state of reduced activity called senescence. However, cancer genes can "take revenge" by revitalizing these cells so they can reproduce again.

The mechanism of regeneration of senescent cells, sometimes called "zombie cells", was only partially understood. Researchers from Rutgers School of Medicine (New Jersey, USA) traced this process in colorectal cancer cells, and believe it is similar to other types of tumors. Medical Xpress writes about it.

"As soon as a cell starts to become cancerous, it starts multiplying very quickly, and this causes senescence. However, when a cell senesces, it often starts to produce a certain protein that helps it get out of senescence," said the study's lead author Ricardo Ivan Martínez-Samudio.

"The next stage of research is to find out whether drugs can target this protein. We want to find a substance that will interact with it and prevent it from binding to other proteins so that these cells remain in a state of aging and do not multiply," said Martinez-Samudio.

The researchers began by studying the progression of cells cultured in petri dishes. They then confirmed their findings in tissues taken from real colon cancer patients.

Scientists have found out that the onset of aging and the exit from it are pre-coded and mediated by the same types of proteins.

The study identified POU2F2 as a critical anti-aging protein and showed its role in the development of rectal cancer. Overexpression and increased activity of POU2F2 are associated with inflammation and cell proliferation, as well as decreased patient survival.

POU2F2 is involved in the development of various types of cancer and may be a suitable drug target.

Any strategy to help prevent aging can help, experts say. A subset of the tissue samples showed gene signatures that kept cells in senescence rather than letting them slip away, and these patients were more likely to survive their cancer than patients whose cells avoided senescence.

The researchers traced the transition from cellular senescence to "awakening" using a technique called multi-ohm profiling, which allowed them to see which genes were turned on and off, and which proteins subsequently became more and more abundant.

Once this method showed that the AP1 transcription factors were particularly active before the cells escaped senescence, the researchers turned off the genes that make these proteins and found that the cells could no longer come back to life and begin to reproduce.

"The body protects itself against certain types of tumors by forcing the cells to completely destroy themselves, rather than downregulating before aging," Martinez-Samudio said.

"We're not entirely sure why this isn't a more common response—perhaps because the destruction of large numbers of continuous cells would create 'holes' in important tissues—but the body prefers aging rather than cell death as a defense against many solid tissue tumors, so we want the protection to work properly," he added.