Pharmacologic inhibition of ATR and ATM offers clinically important distinctions to enhancing platinum or radiation response in ovarian, endometrial, and cervical cancer cells

Gynecol Oncol. 2015 Mar;136(3):554-61. doi: 10.1016/j.ygyno.2014.12.035. Epub 2015 Jan 2.

Abstract

Objective: Significant reductions in gynecologic (GYN) cancer mortality and morbidity require treatments that prevent and reverse resistance to chemotherapy and radiation. The objective of this study was to determine if pharmacologic inhibition of key DNA damage response kinases in GYN cancers would enhance cell killing by platinum-based chemotherapy and radiation.

Methods: A panel of human ovarian, endometrial and cervical cancer cell lines were treated with platinum drugs or ionizing radiation (IR) along with small molecule pharmacological kinase inhibitors of Ataxia telangiectasia mutated (ATM) and ATM and Rad-3-related (ATR).

Results: Pharmacologic inhibition of ATR significantly enhanced platinum drug response in all GYN cancer cell lines tested, whereas inhibition of ATM did not enhance the response to platinum drugs. Co-inhibition of ATM and ATR did not enhance platinum kill beyond that observed by inhibition of ATR alone. By contrast, inhibiting either ATR or ATM enhanced the response to IR in all GYN cancer cells, with further enhancement achieved with co-inhibition.

Conclusions: These studies highlight actionable mechanisms operative in GYN cancer cells with potential to maximize response of platinum agents and radiation in newly diagnosed as well as recurrent gynecologic cancers.

Keywords: ATM; ATR; Cisplatin resistance; DNA damage repair response; Gynecologic cancer; Ionizing radiation.

Publication types

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

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use
  • Apoptosis / drug effects
  • Ataxia Telangiectasia Mutated Proteins / antagonists & inhibitors*
  • Biomarkers, Tumor / antagonists & inhibitors*
  • Cell Line, Tumor
  • Cisplatin / pharmacology*
  • Cisplatin / therapeutic use
  • DNA Damage / drug effects
  • DNA Repair / drug effects
  • Drug Resistance, Neoplasm / drug effects
  • Female
  • Genital Neoplasms, Female / drug therapy*
  • Genital Neoplasms, Female / enzymology
  • Genital Neoplasms, Female / radiotherapy*
  • Humans
  • Morpholines / pharmacology
  • Oxazines / pharmacology
  • Protein Kinase Inhibitors / pharmacology*
  • Pyrones / pharmacology
  • Quinolines / pharmacology

Substances

  • 2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one
  • Antineoplastic Agents
  • Biomarkers, Tumor
  • ETP-46464
  • Morpholines
  • Oxazines
  • Protein Kinase Inhibitors
  • Pyrones
  • Quinolines
  • ATM protein, human
  • ATR protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Cisplatin