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Jekyll and Hyde Protein Prevents as Well as Spreads Cancer

by Bidita Debnath on February 10, 2015 at 11:31 PM

Jekyll and Hyde Protein Prevents as Well as Spreads Cancer
A new research has revealed why a protein that suppresses tumors also causes metastasis.

Scottish author Robert Louis Stevenson tapped into primal fears when he penned "Dr. Jekyll and Mr. Hyde," a 19th century novel about a sinister physician, raising the question, "Can evil and good exist in the same person?"
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As it turns out, cancer researchers are discovering that "good vs. bad" can also exist in the world of molecular genetics and one example is a protein, transforming growth factor beta (TGF-Beta) that suppresses tumor progression in pre-malignant cells, can also lead to the spread of cancer.

It has been a long-time puzzle how and when TGF-Beta switches its functional roles from a tumor suppressor to a metastasis promoter and now, scientists at The University of Texas believe they have an answer.
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The research demonstrates that another protein, known as 14-3-3 zeta, can switch TGF-Beta from suppressing tumors in pre-cancerous cells to promoting metastasis in breast cancer cells, spreading to the bones by changing the TGF-Beta's partner proteins.

Dihua Yu said that TGF-Beta has a dual role as both a tumor suppressor in normal and pre-malignant cells, and a metastasis promoter in late-stage cancer and the molecular mechanism by which TGF-Beta switches its role has long been an unsolved mystery for cancer researchers.

Yu added that TGF-Beta's known critical role in cancer has led to numerous efforts developing TGF-Beta inhibitors for anti-cancer therapeutics, but its penchant for both suppressing tumor progression while serving as a springboard for cancer metastasis has been a major obstacle in the development of anti-TGF-Beta therapies and they have developed a model that proposes that TGF-Beta's complicated nature may be governed by the cellular effects of SMAD's partner proteins.

Yu concluded that because TGF-Beta plays important roles in various physiological functions, it is crucial that we look at how to develop more specific drugs that selectively target TGF-Beta in cancer so as to discourage its ability to cause metastasis while maintaining its tumor suppression abilities in pre-cancerous cells.

The results are published in Cancer Cell.

Source: ANI
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