Mice lacking this protein lived longer and developed fewer and smaller tumors.

Loss of heat-shock factor 1 (HSF1) had a positive effect on cancer response in mice and human cell lines, according to a team from the Whitehead Institute for Biomedical Research.

Previous research noted that levels of heat shock proteins increase in many cancer cells. Examining a mouse model of skin cancer, the researchers found that animals unable to switch on the heat-shock response took five weeks longer to develop tumors than normal mice. The HSF1-deficient mice were also less likely to develop cancer and when they did, had fewer and smaller tumors as well as lived longer, the researchers report.

The team then looked at mice predisposed to develop cancer due to a deficiency of p53. They report that the HSF1-deficient animals again lived tumor-free for dramatically longer.

Through studies in cultured mouse cells, the investigators found further evidence that HSF1 supports the transformation to cancer by orchestrating a variety of basic cell functions including proliferation, survival, protein synthesis, and glucose metabolism.

Finally, the Whitehead team examined the role of HSF1 in normal and cancerous human cells including those derived from the breast, prostate, and cervix. In every case, they found that the cancerous cells, but not the normal cells, were strongly affected by HSF1’s inhibition.

The study will be reported in the September 21 issue of Cell.

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