Retinoids augment thiazolidinedione PPARγ activation in oral cancer cells

Raul Rosas, Seth Buryska, Robert Silver, Beverly Wuertz, Frank Ondrey

Research output: Contribution to journalArticlepeer-review

Abstract

Background/Aim: Head and neck squamous cell carcinoma affects nearly 500,000 people annually. Augmenting PPARγ functional activation is linked with multiple anti-carcinogenic processes in aerodigestive cell lines and animal models. PPARγ/RXRα heterodimers may be key partners in this activation. Materials and Methods: CA 9-22 and NA cell lines were treated with the PPARγ agonist ciglitazone and/or the RXRα agonist 9-cis-retinoic acid. PPARγ functional activation, cellular proliferation, apoptosis activity, and phenotype were subsequently analyzed. Results: Ciglitazone and 9-cis-retinoic acid independently activated PPARγ and down-regulated the carcinogenic phenotype in vitro. Combination treatment significantly augmented these effects, further decreasing proliferation (p<0.0001), and increasing PPARγ functional activation (p<0.0001), apoptosis (p<0.05), and adipocyte differentiation markers (p<0.0001). Conclusion: The efficacy of the combination of ciglitazone and 9-cis-retinoic acid afforded lowering treatment concentrations while maintaining desired therapeutic outcomes, optimistically supporting the feasibility and practicality of this novel treatment option.

Original languageEnglish (US)
Pages (from-to)3071-3080
Number of pages10
JournalAnticancer Research
Volume40
Issue number6
DOIs
StatePublished - Jun 1 2020

Bibliographical note

Funding Information:
The Authors would like to thank Donna Seabloom for comments on the manuscript. This work was funded by the Lion’s 5M Hearing Center Grant (Minnesota) and P30 CA77598-07 (NCI/NIH).

Keywords

  • 9-cis-retinoic acid
  • Ciglitazone
  • Head
  • Neck squamous carcinoma
  • PPARγ
  • Retinoids
  • Thiazolidinedione

PubMed: MeSH publication types

  • Journal Article

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