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Researchers discover second protective role for tumor-suppressor
Date:2/18/2010

b was studying another tumor-suppressing protein called TSC2 that is active in the cellular cytoplasm and found that ATM appeared to be associated with TSC2 activation.

In a series of experiments, the research team uncovered the molecular pathway that begins with ROS activation of ATM which then:

  • Activates the tumor suppressor LKB1, which in turn phosphorylates and activates the AMP kinase (AMPK), a key player in energy sensing and growth factor signaling.

  • AMPK switches on the tumor-suppressor TSC2 (tuberous sclerosis complex 2).

  • TSC2 then suppresses the kinase mTOR (mammalian Target of Rapamycin), which shuts down the mTORC1 signaling pathway, an important regulator of protein creation and cell growth.

  • Because TORC1 suppresses autophagy, when TORC1 is suppressed by TSC2, autophagy is free to occur.

During autophagy, membranes form around organelles in the cytoplasm, which are subsequently digested. Autophagy plays a normal role in cell growth and stability, and is a natural cellular defense mechanism, providing nutrients for a starving cell, for example.

Autophagy also is thought to be a second form of programmed cell death, because it can eventually kill the cell, cannibalizing it and leaving it shot full of cavities. Whether autophagy is activated as a survival mechanism in response to ROS or as an ATM-driven programmed cell death remains to be explored, the authors noted.

Even so, the study links oxidative stress to a key metabolic pathway activated by ATM that integrates damage response pathways with energy signaling, protein synthesis and cell survival.


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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert

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