Wednesday, July 22, 2009

Cancer and Aging: the Yin and Yang of Cells?

The idea that cancer and aging may be related or even share some common features was not a conclusion intuitively reached by armchair thinkings. Although there is a clear correlation between age and the frequency of onset of cancer, on the cellular level, it is quite hard to imagine what cancer, characterized by incessant cell proliferation, could have anything to do with aging, which suggests a transformation of cells into more lethargic state in most circumstances. However, from the 1960s until now, the parallel study of both phenomena and the communication between them led scientists to the recognition that cancer and aging share many biological grounds.

Finkel et al. 2007 gave pretty thorough a review of the common biology between cancer and aging. They even took pain to mention several historical aspects, pointing to the once nebulous clues found in laboratories that suggested the link between cancer and aging. Indeed, the clues came from many fields. Cell culturists Leonard Hayflick found the upper limit of cell division when he was in the middle of his subculturing routines and suggested there must be a shared mechanisms to determine the fate of the cells, either aging or proliferative malignancy. p53, an initiator of cellular senescence, was initially discovered first as a repressor of oncogenesis. Telomere, the once alleged determinator of life span, was proved to be vital to most of the cancer cells as well. As the author said for several times, this may mean that a treatment for cancer may involve accelerating aging processes. However, cancer and aging are not clear-cut opposites sitting at the two ends in the cellular fate. They displayed similar behaviors as well. They both lack sufficient maintenance for genome stability, and they do not keep enough activity of autophagy for waste management. This shared shortage of cancer and senescent cells may suggest a common ground to slow down cancer and aging by one intervention.

Those authors thanked Henrietta for her inadvertent contribution of her cervical cancer cells, denoted later as HeLa cells. They probably could have added the importance of many fetal cells raised in cell cultures as well. Although those cells could not compete with HeLa cells’ longevity in the dish, they nevertheless provided the sheer contrast in cellular behavior between normal cells and cancer cells, illuminating the first hint about the existence of an underlying mechanism that determines cellular mortality (aging) or the escape from it (cancer).

Finkel, T., M. Serrano, and M. A. Blasco. "The Common Biology of Cancer and Ageing." Nature 448, no. 7155 (2007): 767-74.

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