Gene interplay may govern spread of cancer.Cancer is like a deadly infection. The body can often handle the problem, or physicians can treat it, if it confines itself to a small area. If it spreads, however, disaster usually follows. Scientists now suggest that a gene, KAI1, that can suppress the dispersal of tumor cells is under the control of p53, a gene often mutated in cancers. In 1995, scientists observed that adding KAI1 to rat prostate tumor cells prevented the cancer from spreading to the animals' lungs, as it normally does. Since then, they have also found that as human prostate, breast, bladder, pancreatic, and lung cancers lung cancer, cancer that originates in the tissues of the lungs. Lung cancer is the leading cause of cancer death in the United States in both men and women. Like other cancers, lung cancer occurs after repeated insults to the genetic material of the cell. grow, tumor cells frequently make less of KAI1's protein--even though the gene isn't mutated. Kounosuke Watabe of Southern Illinois University Southern Illinois University, main campus at Carbondale; state supported; coeducational; est. 1869, opened 1874 as a normal school, renamed 1947. It has a center for archaeological investigation and a fisheries research laboratory. There is also a campus at Edwardsville. School of Medicine in Springfield and his colleagues recently identified a DNA sequence DNA sequence Genetics The precise order of bases–A,T,G,C–in a segment of DNA, gene, chromosome, or an entire genome. See Base pair, Base sequence analysis, Chromosome, Gene, Genome. called a promoter region around KAI1. Proteins that attach to this region control the gene's activity. Unexpectedly, KAI1's promoter resembles promoters that p53's protein binds. Normally turned on by DNA DNA: see nucleic acid. DNA or deoxyribonucleic acid One of two types of nucleic acid (the other is RNA); a complex organic compound found in all living cells and many viruses. It is the chemical substance of genes. damage, p53 safeguards the body against cancer in several ways. Its protein can temporarily halt the division of cells, giving them time to fix mutations. The protein can also induce the suicide of cells damaged beyond repair. Given p53's protective powers, it's not surprising that it is the gene most frequently found mutated in tumors. More than half of all cancers have a disabled p53. Watabe and his colleagues demonstrated that p53's protein does indeed bind to KAI1's promoter region, suggesting an unanticipated role for p53 in suppressing the spread of cancer. In the Sept. 15 Proceedings of the National Academy of Sciences The Proceedings of the National Academy of Sciences of the United States of America, usually referred to as PNAS, is the official journal of the United States National Academy of Sciences. , they also report that adding a working copy of p53 to cells significantly increases production of KAI1's protein. They propose that mutations in p53 explain why cancer cells cells once believed to be peculiar to cancers, but now know to be epithelial cells differing in no respect from those found elsewhere in the body, and distinguished only by peculiarity of location and grouping. See also: Cancer stop producing KAI1's protein. The function of that cell-surface protein "is not well-understood. It is probably involved in cell adhesion Cellular adhesion is the binding of a cell to another cell or to a surface or matrix. Cellular adhesion is regulated by specific adhesion molecules that interact with molecules on the opposing cell or surface. , but that's about all we know," notes Watabe. |
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