Abstract：
:Following DNA damage, human cells arrest primarily in the G(1) and G(2) phases of the cell cycle. Here, we show that after irradiation, human cancer cells with targeted deletion of PTEN or naturally occurring PTEN mutations can exert G(1) and G(2) arrests but are unable to arrest in size. Pharmacological inhibition of phosphoinositol-3-kinase or mTOR in PTEN(-/-) cells restored the size arrest, whereas siRNA-mediated depletion of TSC2 in PTEN(+/+) cells attenuated the size arrest. Radiation treatment potentiated Akt activation in PTEN(-/-) but not PTEN(+/+) cells. Finally, abrogation of the size arrest via PTEN deletion conferred radiosensitivity both in vitro and in vivo. These results identify a new tumor suppressor gene-regulated, DNA damage-inducible arrest that occurs simultaneously with the G(1) and G(2) arrests but is genetically separable from them. We suggest that aberrant regulation of cell size during cell cycle arrest may be important in human cancer pathogenesis.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Lee C,Kim JS,Waldman Tdoi
10.1158/0008-5472.CAN-04-1767subject
Has Abstractpub_date
2004-10-01 00:00:00pages
6906-14issue
19eissn
0008-5472issn
1538-7445pii
64/19/6906journal_volume
64pub_type
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