Non Stop Cancer Cell Division Could Be Explained By The Help Of A New Telomere Discovery
The discovery that RNA is present in telomeres, the repeated DNA-protein complexes at the end of chromosomes that progressively shorten every time a cell divides puts into scrutiny our understanding of how telomeres behave and may also provide a new way of attack to stop telomere renewal in cancer cells.
The DNA in the chromosome acts like a sort of instruction manual for the cell. Genetic information is transcribed into segments of RNA that then go out into the cell and carry out a variety of tasks such as making proteins, catalyzing chemical reactions, or fulfilling structural roles. It was thought that telomeres were “silent” — that their DNA was not transcribed into strands of RNA. The researchers have turned this theory on its head by discovering telomeric RNA and showing that this RNA is transcribed from DNA on the telomere.
Inside the cell nucleus, all our genetic information is located on twisted, double stranded molecules of DNA which are packaged into chromosomes. At the end of these chromosomes are telomeres, zones of repeated chains of DNA that are often compared to the plastic tips on shoelaces because they prevent chromosomes from fraying, and thus genetic information from getting scrambled when cells divide. The telomere is like a cellular clock, because every time a cell divides, the telomere shortens. After a cell has grown and divided a few dozen times, the telomeres turn on an alarm system that prevents further division. If this clock doesn’t function right, cells either end up with damaged chromosomes or they become “immortal” and continue dividing endlessly — either way it’s bad news and leads to cancer or disease. Understanding how telomeres function, and how this function can potentially be manipulated, is thus extremely important.
Why is this important” In embryonic cells (and some stem cells), an enzyme called telomerase rebuilds the telomere so that the cells can keep dividing. Over time, this telomerase dwindles and eventually the telomere shortens and the cell becomes inactive. In cancer cells, the telomerase enzyme keeps rebuilding telomeres long past the cell’s normal lifetime. The cells become “immortal”, endlessly dividing, resulting in a tumor. Researchers estimate that telomere maintenance activity occurs in about 90% of human cancers. But the mechanism by which this maintenance takes place is not well understood. The researchers discovered that the RNA in the telomere is regulated by a protein in the telomerase enzyme. Their discovery may thus uncover key elements of telomere function.
“It’s too early to give yet a definitive answer,” to whether this could lead to new cancer therapies, notes Joachim Lingner, an Associate Professor at the EPFL (Ecole Polytechnique Fédérale de Lausanne) and senior author on the paper done at at the Swiss Institute for Experimental Cancer Research (ISREC) in collaboration with the University of Pavia. “But the experiments published in the paper suggest that telomeric RNA may provide a new target to attack telomere function in cancer cells to stop their growth.”
Funding for this research was provided in part by the Swiss National Science Foundation NCCR “Frontiers in Genetics”.
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