Roflumilast enhances cisplatin-sensitivity and reverses cisplatin-resistance of ovarian cancer cells via cAMP/PKA/CREB-FtMt signalling axis

Cell Prolif. 2018 Oct;51(5):e12474. doi: 10.1111/cpr.12474. Epub 2018 Aug 2.

Abstract

Objective: We previously demonstrated the roflumilast inhibited cell proliferation and increased cell apoptosis in ovarian cancer. In this study, we aimed to investigate the roles of roflumilast in development of cisplatin (DDP)-sensitive and -resistant ovarian cancer.

Methods: OVCAR3 and SKOV3 were selected and the corresponding DDP-resistant cells were constructed. Cell viability, proliferation, apoptosis, cycle were performed. Expression cAMP, PKA, CREB, phosphorylation of CREB and FtMt were detected. The roles of roflumilast in development of DDP-sensitive and -resistant ovarian cancer were confirmed by xenograft model.

Results: Roflumilast + DDP inhibited cell proliferation, and induced cell apoptosis and G0/G1 arrest in OVCAR3 and SKOV3 cells, roflumilast induced expression of FtMt, the activity of cAMP and PKA and phosphorylation of CREB in ovarian cancer cells and the above-effect were inhibited by H89. Downregulation of CREB inhibited the roflumilast-increased DDP sensitivity of ovarian cancer cells, and the roflumilast-induced FtMt expression and phosphorylation of CREB. Also, roflumilast reversed cisplatin-resistance, and induced expression of FtMt and activation of cAMP/PKA/CREB in DDP-resistant ovarian cancer cells. Similarly, treated with H89 or downregulation of CREB inhibited the changes induced by roflumilast. In vivo, roflumilast inhibited the development of SKOV3 or SKOV3-DDP-R xenograft models.

Conclusions: Roflumilast enhanced DDP sensitivity and reversed the DDP resistance of ovarian cancer cells via activation of cAMP/PKA/CREB pathway and upregulation of the downstream FtMt expression, which has great promise in clinical treatment.

MeSH terms

  • Aminopyridines / pharmacology*
  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects
  • Benzamides / pharmacology*
  • Cell Cycle Checkpoints / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cisplatin / pharmacology*
  • Cyclic AMP / metabolism*
  • Cyclic AMP Response Element-Binding Protein / metabolism*
  • Cyclic AMP-Dependent Protein Kinases / metabolism*
  • Cyclopropanes / pharmacology
  • Down-Regulation / drug effects
  • Drug Resistance, Neoplasm / drug effects*
  • Female
  • Ferritins / metabolism*
  • G1 Phase / drug effects
  • Humans
  • Mitochondrial Proteins / metabolism*
  • Ovarian Neoplasms / drug therapy*
  • Ovarian Neoplasms / metabolism
  • Resting Phase, Cell Cycle / drug effects
  • Signal Transduction / drug effects

Substances

  • Aminopyridines
  • Antineoplastic Agents
  • Benzamides
  • CREB1 protein, human
  • Cyclic AMP Response Element-Binding Protein
  • Cyclopropanes
  • Mitochondrial Proteins
  • mitochondrial ferritin, human
  • Roflumilast
  • Ferritins
  • Cyclic AMP
  • Cyclic AMP-Dependent Protein Kinases
  • Cisplatin

Associated data

  • GENBANK/ab66111
  • GENBANK/ab124889
  • GENBANK/ab32096
  • GENBANK/BS12478
  • GENBANK/BS13278