Key to TGF-Beta Growth Stimulation Found

To explain this apparent paradox, researchers at Vanderbilt University (Nashville, TN, USA; www.vanderbilt.edu) genetically engineered a line of cells lacking the TGF-b signaling proteins Rho-ROCK. They found that these cells, which derived from a line normally not affected by TGF-b, were readily transformed by the growth factor. Addition of extraneous Rho-Rock proteins restored the inhibition to TGF-b growth stimulation. These findings were published in the December 1, 2003, online edition of the Proceedings of the [U.S.] National Academy of Sciences.

"TGF-b usually causes cell growth inhibition; however, many solid tumors overexpress TGF-b and the cells are not inhibited at all--in fact, sometimes they grow faster than normal as a result of TGF-b signaling,” explained first author Dr. Neil A. Bhowmick, assistant professor of urologic surgery at Vanderbilt University. "Perhaps inactivation of this pathway is a way that cancer cells override the normal growth-suppressing activity of TGF-b.”




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