Human non‑small cell lung cancer cells can be sensitized to camptothecin by modulating autophagy

Int J Oncol. 2018 Nov;53(5):1967-1979. doi: 10.3892/ijo.2018.4523. Epub 2018 Aug 14.

Abstract

Lung cancer is a prevalent disease and is one of the leading causes of mortality worldwide. Despite the development of various anticancer drugs, the prognosis of lung cancer is relatively poor. Metastasis of lung cancer, as well as chemoresistance, is associated with a high mortality rate for patients with lung cancer. Camptothecin (CPT) is a well-known anticancer drug, which causes cancer cell apoptosis via the induction of DNA damage; however, the cytotoxicity of CPT easily reaches a plateau at a relatively high dose in lung cancer cells, thus limiting its efficacy. The present study demonstrated that CPT may induce autophagy in two human non‑small cell lung cancer cell lines, H1299 and H460. In addition, the results of a viability assay and Annexin V staining revealed that CPT-induced autophagy could protect lung cancer cells from programmed cell death. Conversely, the cytotoxicity of CPT was increased when autophagy was blocked by 3-methyladenine treatment. Furthermore, inhibition of autophagy enhanced the levels of CPT-induced DNA damage in the lung cancer cell lines. Accordingly, these findings suggested that autophagy exerts a protective role in CPT-treated lung cancer cells, and the combination of CPT with a specific inhibitor of autophagy may be considered a promising strategy for the future treatment of lung cancer.

MeSH terms

  • Adenine / administration & dosage
  • Adenine / analogs & derivatives
  • Adenine / pharmacology
  • Amino Acid Chloromethyl Ketones / pharmacology
  • Antineoplastic Agents, Phytogenic / administration & dosage
  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology
  • Apoptosis / drug effects
  • Autophagy / drug effects*
  • Camptothecin / administration & dosage
  • Camptothecin / pharmacology*
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / pathology
  • Caspase Inhibitors / pharmacology
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • DNA Damage / drug effects
  • Dose-Response Relationship, Drug
  • Drug Resistance, Neoplasm / drug effects
  • Histones / metabolism
  • Humans
  • Inhibitory Concentration 50
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology

Substances

  • Amino Acid Chloromethyl Ketones
  • Antineoplastic Agents, Phytogenic
  • Caspase Inhibitors
  • H2AX protein, human
  • Histones
  • benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
  • 3-methyladenine
  • Adenine
  • Camptothecin