Insights into 4E-BP1 and p53 mediated regulation of accelerated cell senescence

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Abstract

Senescence is a valid tumor suppressive mechanism in cancer. Accelerated cell senescence describes the growth arrested state of cells that have been treated with anti-tumor drugs, such as doxorubicin that induce a DNA damage response. Discodermolide, a microtubule-stabilizing agent, is a potent inducer of accelerated cell senescence. Resistance to discodermolide is mediated via resistance to accelerated cell senescence, and is associated with reduced expression of the mTORC1 substrate, 4E-BP1 and increased expression of p53 [1]. Although the association of p53 with senescence induction is well-characterized, senescence reversion in the presence of high expression of p53 has not been well-documented. Furthermore, studies addressing the role of mTOR signaling in regulating senescence have been limited and recent data implicate a novel, senescence-associated role for 4E-BP1 in crosstalk with the transcription factor p53. This research perspective will address these somewhat contradictory findings and summarize recent research regarding senescence and mTORC1 signaling. © Chao et al.

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Chao, S. K., Horwitz, S. B., & McDaid, H. M. (2011). Insights into 4E-BP1 and p53 mediated regulation of accelerated cell senescence. Oncotarget, 2(1–2), 89–98. https://doi.org/10.18632/oncotarget.221

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