Apoptosis of metastatic prostate cancer cells by a combination of cyclin-dependent kinase and AKT inhibitors

Int J Biochem Cell Biol. 2009 Mar;41(3):595-602. doi: 10.1016/j.biocel.2008.07.013. Epub 2008 Jul 31.

Abstract

Effective treatments for advanced prostate cancer are much needed. Toward this goal, we show apoptosis and impaired long-term survival of androgen-independent prostate cancer cells (PC3 and PC3 derivatives) co-treated with the cyclin-dependent kinase (CDK) inhibitor roscovitine and an AKT inhibitor (LY294002 or API-2). Apoptosis of PC3 cells by the drug combination required caspase-9 but not caspase-8 activity and thus is mitochondria-dependent. Roscovitine reduced amounts of the caspase inhibitor XIAP, and API-2 increased amounts of the BH3-only protein Bim. PC3 cells apoptosed when co-treated with API-2 and either cdk9 siRNA, dominant-negative cdk9, or the cdk9 inhibitor DRB; they did not apoptose when co-treated with API-2 and XIAP siRNA. Bax accumulated in mitochondria in response to API-2, whereas release of cytochrome c from mitochondria required both API-2 and roscovitine. We suggest that roscovitine elicits events that activate Bax once it translocates to mitochondria and that inactivation of cdk9 signals these events and the down-regulation of XIAP. Collectively, our data show apoptosis of prostate cancer cells by a drug combination and identify Bax activation as a basis of cooperation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis Regulatory Proteins / genetics
  • Apoptosis Regulatory Proteins / metabolism*
  • Bcl-2-Like Protein 11
  • Caspase 9 / genetics
  • Caspase 9 / metabolism*
  • Cell Line, Tumor
  • Chlorpropamide / analogs & derivatives
  • Chlorpropamide / pharmacology
  • Chromones / pharmacology
  • Cyclin-Dependent Kinase 9 / genetics
  • Cyclin-Dependent Kinase 9 / metabolism*
  • Cyclin-Dependent Kinases / antagonists & inhibitors
  • DNA / biosynthesis
  • Dichlororibofuranosylbenzimidazole / pharmacology
  • Drug Synergism
  • Humans
  • Male
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Mitochondria / drug effects
  • Mitochondria / metabolism*
  • Mitochondria / pathology
  • Morpholines / pharmacology
  • Nucleic Acid Synthesis Inhibitors / pharmacology
  • Prostatic Neoplasms / drug therapy*
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / pathology
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism*
  • Proto-Oncogene Proteins c-akt / antagonists & inhibitors
  • Purines / pharmacology
  • RNA, Small Interfering / genetics
  • Roscovitine
  • X-Linked Inhibitor of Apoptosis Protein / metabolism

Substances

  • API 2
  • Apoptosis Regulatory Proteins
  • BCL2L11 protein, human
  • Bcl-2-Like Protein 11
  • Chromones
  • Membrane Proteins
  • Morpholines
  • Nucleic Acid Synthesis Inhibitors
  • Proto-Oncogene Proteins
  • Purines
  • RNA, Small Interfering
  • X-Linked Inhibitor of Apoptosis Protein
  • Roscovitine
  • 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
  • Dichlororibofuranosylbenzimidazole
  • DNA
  • Proto-Oncogene Proteins c-akt
  • Cyclin-Dependent Kinase 9
  • Cyclin-Dependent Kinases
  • Caspase 9
  • Chlorpropamide