Aiding and abetting: a longevity gene also promotes cancer.A gene that helps organisms survive damage to their cells can also shorten their lives by fostering tumors, tests on mice and human-cell lines show.
The gene, called heat-shock factor 1 (Hsf1), doesn't itself trigger cancer. Instead, it appears to help cells survive the stressful process of becoming cancerous, which involves extensive damage to DNA DNA: see nucleic acid.
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. and the malfunctioning of many proteins.
The discovery reveals a dark side of Hsf1, which is known to promote longevity in labgrown roundworms and to protect people against the brain-cell damage of Alzheimer's and Parkinson's diseases. Some researchers are developing drugs that might ease the brain diseases by boosting Hsf1 activity.
Now it appears that hindering Hsf1 could be a new way to combat cancer.
The new study "does bring [Hsf1] forward as a possible therapeutic target" in cancer research, says team member Luke Whitesell of the Whitehead Institute Founded in 1982, the Whitehead Institute for Biomedical Research is a non-profit research and teaching institution located in Cambridge, Massachusetts. The Whitehead Institute was founded as a fiscally independent entity from Massachusetts Institute of Technology, and its members for Biomedical Research Biomedical research (or experimental medicine), in general simply known as medical research, is the basic research or applied research conducted to aid the body of knowledge in the field of medicine. in Cambridge, Mass. However, Whitesell cautions that more work is needed before scientists can develop cancer drugs that exploit this discovery.
The cancer-facilitating effects of Hsf1 may stem from its role as the ringleader ring·lead·er
A person who leads others, especially in illicit or informal activities.
a person who leads others in illegal or mischievous actions
Noun 1. of so-called heat-shock proteins. Stresses such as excessive heat, exposure to free radicals, or a lack of oxygen can damage a cell's molecular machinery. When that happens, heat-shock proteins can keep a cell healthy by either fixing or expelling ex·pel
tr.v. ex·pelled, ex·pel·ling, ex·pels
1. To force or drive out: expel an invader.
2. damaged cellular components.
Hsf1 activates this repair system by boosting the activity of heat-shock proteins. The gene also regulates proteins involved in energy production and cell proliferation, which might also contribute to the gene's ability to aid cancer formation.
Scientists had previously observed that tumor cells often have abnormally high quantities of heat-shock proteins. White-sell and his colleagues wondered whether those proteins had a role in keeping the tumor cells alive.
The researchers tested their idea by inducing skin cancer in 29 normal mice and 23 mice engineered to lack Hsf1. The mice without Hsf1 had a significantly lower incidence of cancer than did the genetically normal group, the team reported in the Sept. 21 Cell. After 55 weeks, more than 90 percent of the Hsf1-free mice were still alive, while only about 35 percent of the normal mice had survived.
When Whitesell's team repeated the experiment on mice with a cancer-causing genetic mutation Noun 1. genetic mutation - (genetics) any event that changes genetic structure; any alteration in the inherited nucleic acid sequence of the genotype of an organism
chromosomal mutation, mutation , about 75 percent of the mice without Hsf1 survived at least 90 weeks, while none of the mice with intact Hsf1 genes did.
Some cancers appear to have a similar dependence on the gene. The researchers blocked Hsf1 activity in a variety of human-cancer cells growing in the lab. In all cases, most of the 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 died. Healthy human cells growing in similar conditions showed no ill effects from blocking the gene's activity, reinforcing the point that Hsf1 is critical only for cells under duress duress (dy`rĭs, d`–, d .
"I thought the results were very clear," comments Stephen J. Elledge of Harvard Medical School Harvard Medical School (HMS) is one of the graduate schools of Harvard University. It is a prestigious American medical school located in the Longwood Medical Area of the Mission Hill neighborhood of Boston, Massachusetts. in Boston, who wrote a commentary on the work for Cell. "This [gene] has a major role in affecting tumor formation."