From: Subject: Researchers find molecular 'brake' to cell death Date: Fri, 30 Jun 2006 09:50:37 +0200 MIME-Version: 1.0 Content-Type: multipart/related; type="text/html"; boundary="----=_NextPart_000_0000_01C69C2A.A3BCB290" X-MimeOLE: Produced By Microsoft MimeOLE V6.00.2900.2869 This is a multi-part message in MIME format. ------=_NextPart_000_0000_01C69C2A.A3BCB290 Content-Type: text/html; charset="Windows-1252" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.eurekalert.org/pub_releases/2006-06/uotm-rfm062706.php Researchers find molecular 'brake' to cell = death

Public = release date:=20 29-Jun-2006
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Contact: Scott Merville
sdmervil@mdanderson.org
71= 3-792-0661
University of = Texas M. D.=20 Anderson Cancer Center

Researchers find molecular 'brake' to cell death

Discovery could yield new target for future = therapies

EMBARGOED FOR RELEASE UNTIL THURSDAY, JUNE 29 AT 12 PM EDT=20

HOUSTON - Researchers at The University of Texas M. D. Anderson = Cancer Center=20 have significantly refined the scientific understanding of how a cell = begins the=20 process of self-destruction - an advance they say may help in the design = of more=20 targeted cancer therapies.

In the June 30 issue of the journal Cell, the research team found = that a=20 natural "brake" exists in a cell to prevent it from undergoing = apoptosis, or=20 programmed cell death, and they say that optimal anti-cancer therapies = should=20 take a two-pronged approach to overriding this brake in order to force a = tumor=20 cell to die. Very few drugs do this now, they say.

The discovery "demonstrates that apoptosis is more complicated than = had been=20 believed, and consequently harder to achieve," says the study's lead = author,=20 Dean G. Tang, Ph.D., associate professor in the Department of = Carcinogenesis in=20 the Science Park Research Division of M. D. Anderson in Smithville, = Texas.

Apoptosis can occur when a cell has reached its lifespan, and so is=20 "programmed" to die, or is initiated when a cell is damaged beyond = repair or=20 infected by a virus. Apoptosis is rare in cancer because tumor cells = have=20 adapted biological pathways to circumvent cell death, so many = anti-cancer=20 therapies focus on inducing apoptosis in these cells, Tang says.

But the notion of how to push cancer cells to die has been flawed, = Tang says.=20 These new findings "overturn a scientific dogma so long accepted that it = has=20 become a textbook standard when talking about apoptosis," he = continues.

Researchers agree that the seminal event that leads to initiation of=20 apoptosis is the release of a key protein known as cytochrome c (CC) = from a=20 cell's mitochondria, the organelle's energy storehouse. These molecules = then=20 bind to another protein called Apaf-1 in the cell cytoplasm, and = together they=20 form a scaffolding "death wheel" to activate enzymes called caspases = that shred=20 a cell apart.

But what they also believed is that a cell needs extra energy from = ATP to=20 undergo apoptosis, and that this extra energy was produced from the = "pools" of=20 free nucleotides that exist in the cell cytoplasm. Nucleotides are the = primary=20 structural chemical units that make up DNA, RNA and proteins, and they = combine=20 to play a variety of roles in the cell, such as formation of ATP.

However, through a series of biological and biochemical experiments, = Tang and=20 his research team found that adding ATP to a cancer cell could = potentially=20 impede apoptosis. They discovered that these nucleotide pools, in fact, = act not=20 to promote apoptosis through production of ATP, but to hinder it. They = are=20 "pro-survival factors" that prevent CC, when released from the = mitochondria,=20 from "seeing" Apaf-1 in the cytoplasm, Tang says.

"When we induced some cell stress and damage, the low levels of CC = that came=20 out from the mitochondria were ineffective because they are sequestered = by an=20 ocean of free nucleotides and ATP," he says. "No one had ever realized = this kind=20 of barrier existed to impede apoptosis."

They found that cell mitochondria needed to release a large and = sustained=20 volume of CC to overcome this nucleotide barrier, and they also found = evidence=20 that as soon as the release of CC increases, another mechanism kicks in = that=20 simultaneously begins to reduce the size of the nucleotide pool to allow = CC to=20 bind to Apaf-1, Tang says.

The researchers say this kind of strategy makes sense for the cell, = because=20 it acts like a biological fail-safe system to protect against the errant = release=20 of CC from malfunctioning mitochondria. A large pool of free nucleotides = along=20 with complete ATP molecules normally exists in a healthy cell so that = just a=20 little CC could not mistakenly push the cell to self destruct, Tang = says. "When=20 CC is still limited in the cell, perhaps through an accidental release, = the=20 nucleotide pool will neutralize the CC so that the cell can stay alive," = he=20 says. "So, in a way, it takes a large amount of CC to convince the cell = that the=20 damage is real, and that is what you see when cardiac cells die after a = heart=20 attack, for example."

This finding has direct implications for anti-cancer therapy, Tang = says,=20 suggesting how current therapy could be both inefficient and lead to = resistance=20 in a cell.

"Many cancer drugs focus on pushing the mitochondria to release CC, = and not=20 on reducing the nucleotide pool, and our new model suggests that = decreasing this=20 pool is essential to produce sensitivity in cancer cells to apoptosis," = Tang=20 says.

Cancers that quickly become resistant to therapy, such as melanoma = and=20 ovarian tumors, do so because they have found ways to prevent = mitochondria from=20 releasing a lot of CC, he says. Tumor cells also don't want to decrease = their=20 nucleotide pool, because they need ATP for continued functioning, he = says.

"An optimal cancer therapy should combine both strategies," Tang = says. "They=20 should maximize release of CC and maximize the decrease of nucleotide=20 levels."

Some chemotherapy drugs, like paclitaxel, cisplatin and etoposide, = appear,=20 coincidentally and perhaps inadvertently, to do both, and are very = effective for=20 specific cancers, he says. "But based on these new findings, we now have = a new=20 theoretical approach that can be used to help in the design of more = targeted=20 chemotherapy drugs," Tang says. "This will change the way that = scientists now=20 think about the role of nucleotides in cancer therapy."

###

The study was funded by grants from the National Institutes of = Health, the=20 American Cancer Society, Department of Defense, and the American Heart=20 Association.

Co-authors from the study include M. D. Anderson researchers Dhyan = Chandra,=20 Ph.D., Mary Ayres, Ph.D., and Varsha Gandhi, Ph.D.; Shawn B. Bratton, = Ph.D., and=20 Maria D. Person, Ph.D., from the University of Texas at Austin; Yanan = Tian,=20 Ph.D., from Texas A&M University; and Angel G. Martin, Ph.D., and = Howard O.=20 Fearnhead, Ph.D., from the National Cancer Institute.

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