Research Report: Stress signal in cancer cells aids tumor growth

Lynne Friedmann is a science writer based in Solana Beach.

By Lynne Friedmann

UCSD School of Medicine researchers say a “stress response” mechanism used by normal cells to cope with harsh or demanding conditions is exploited by cancer cells.

Inside all cells, the endoplasmic reticulum (ER) is a protein-making factory. Increased physiological demands or disease can cause proteins to misfold and accumulate in the ER. When this occurs, cells initiate a ER stress response which attempts to reset normal ER balance.

For normal cells, the ER stress response is transient. Tumor cells, however, produce an on-going ER stress response. This triggers an inflammatory response in the surrounding environment that so occupies macrophages that they lose the ability to help the immune system in rejecting the tumor.

The findings appear in the Proceedings of the National Academy of Sciences. News release at bit.ly/hWcZhZ.

Bone-munching worms

Worms that dine on whale carcasses at the bottom of the ocean may be far more ancient than scientists previously thought.

Discovered less than a decade ago, but since identified in other oceans, Osedax “boneworms” have been documented mainly living upon whale carcasses that fall to the ocean floor.

Curious if boneworms lives off of other marine species, a research team led by Scripps Institution of Oceanography at UCSD used remotely operated vehicles to deploy tuna and wahoo bones, as well as shark cartilage inside wire cages at a depth of more than 3,000 feet in waters off Monterey, Calif. Five months later, the cages were retrieved and Osedax was found living on the fish bones.

The finding supports a hypothesis that bone-eating Osedax may have evolved during the Cretaceous period, well before the dawn of marine mammals.

The findings appear in Biology Letters, a Royal Society journal. News release at bit.ly/fl3h9q.

Regulating fat cells development

Scientists at The Scripps Research Institute and collaborating institutions seeking to understand how fat cells form have identified a key regulator of fat cell development that may provide a target for obesity and diabetes drugs.

The finding involves a protein (TLE3) that acts as a dual switch to turn on signals that stimulate fat cell formation and turn off those that keep fat cells from developing. TLE3 works in partnership with a protein that is already the target of several diabetes drugs, but that therapy has been plagued by serious side effects.

To test whether TLE3 might provide an alternative target for diabetes drugs, engineered mice that produce higher-than-normal amounts of human TLE3 were fed a high-fat diet. Normally this would result in insulin resistance and changes in glucose regulation, both risk factors for diabetes. But the engineered mice proved more insulin-sensitive and had better glucose metabolism than control mice fed the same diet.

The findings appear in the journal Cell Metabolism. News release at bit.ly/f4qjoe.

Related posts:

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  3. Research Report: A ‘twist’ found in tumor metastasis
  4. Research Report: Ever heard of the ‘couch potato mouse’?
  5. Research Report: Scripps Research Institute team finds surprising view of brain formation

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Posted by Staff on Apr 20, 2011. Filed under Columns, Editorial Columns, Health & Science, Research Report. You can follow any responses to this entry through the RSS 2.0. You can leave a response or trackback to this entry

1 Comment for “Research Report: Stress signal in cancer cells aids tumor growth”

  1. How can we prevent this problem? Is there any alternate way to prevent this problem?

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