Warning: Undefined array key "mm" in /www/wwwroot/www.ai-bt.com/si.php on line 10 Deprecated: trim(): Passing null to parameter #1 ($string) of type string is deprecated in /www/wwwroot/www.ai-bt.com/si.php on line 10 Cellular quiescence caused by the Mdm2 inhibitor nutlin-3A.

Literature DB >> 19855165

Cellular quiescence caused by the Mdm2 inhibitor nutlin-3A.

Lioubov G Korotchkina¹, Zoya N Demidenko, Andrei V Gudkov, Mikhail V Blagosklonny.

Abstract

Cellular senescence is characterized by irreversible loss of proliferative potential and a large, flat cell morphology. Ectopic p21 and doxorubicin induced cellular senescence in HT1080 and WI-38-tert cell lines. In the same cell lines, the Mdm2 inhibitor nutlin-3a induced p53 but, unexpectedly, caused quiescence (reversible arrest) with a small cell morphology. We discuss that Mdm antagonists could be used in combination with chemotherapy to reversibly arrest normal cells, thus protecting them during chemotherapy of cancer (cyclotherapy).

Entities: Chemical Disease Gene

Mesh：

Substances：

Year: 2009 PMID： 19855165 DOI： 10.4161/cc.8.22.10121

Source DB: PubMed Journal: Cell Cycle ISSN： 1551-4005 Impact factor: 4.534

Keyword Cloud
Cited

42 in total

Cellular quiescence caused by the Mdm2 inhibitor nutlin-3A.

Review 1. Staying alive: metabolic adaptations to quiescence.

2. An indirect role for ASPP1 in limiting p53-dependent p21 expression and cellular senescence.

3. Paradoxical suppression of cellular senescence by p53.

4. Persistent p21 expression after Nutlin-3a removal is associated with senescence-like arrest in 4N cells.

5. HdmX overexpression inhibits oncogene induced cellular senescence.

Review 6. Cellular senescence: from growth arrest to immunogenic conversion.

7. Another "Janus paradox" of p53: induction of cell senescence versus quiescence.

8. Decision-making by p53 and mTOR.

9. New biomarkers probing depth of cell senescence assessed by laser scanning cytometry.

10. Pseudo-DNA damage response in senescent cells.