A novel compound LingH2-10 inhibits the growth of triple negative breast cancer cells in vitro and in vivo as a selective inverse agonist of estrogen-related receptor α

Biomed Pharmacother. 2017 Sep:93:913-922. doi: 10.1016/j.biopha.2017.07.016. Epub 2017 Jul 13.

Abstract

Unlike other breast cancer subtypes, targeted therapies for triple negative breast cancer (TNBC) have yet to progress past clinical trial stage to approval. Accumulating evidences demonstrated that expression of estrogen-related receptor alpha (ERRα) indicated worse prognosis and correlated with poor outcome in breast cancers including TNBC. Therefore, ERRα modulators/regulators may be potential in the therapeutic treatment of breast cancers. In the current study, we presented a novel compound LingH2-10 that bound to ERRα, as identified using a time-resolved fluorescence resonance energy transfer assay (TR-FRET) with the IC50 value of 0.64±0.12μM. Further, functional activity was determined by transient transfection luciferase reporter assay in order to validate the utility of the binding affinity in a cellular context. LingH2-10 showed selective inhibition on ERRα transcriptional activity with the IC50 value of 0.58±0.09μM in cell-based luciferase reporter assay. Moreover, representative in vitro results showed that LingH2-10 suppressed the proliferation of various human cancer cells, and inhibited the migration of triple negative breast cancer cell MDA-MB-231. In addition, our results demonstrated that well known ERRα target genes such as PDK4, Osteopontin and pS2, were all significantly down modulated by LingH2-10. In vivo experiments showed that LingH2-10 (30mg/kg, every other day) observably suppressed the growth of MDA-MB-231 xenograft tumors by 42.02% compared to untreated xenograft tumors. Taken together, all these data suggested that LingH2-10, as a selective inverse agonist of ERRα, was a lead compound of anti-cancer agents for treating TNBC patients.

Keywords: Estrogen-related receptor α; Inverse agonist; Triple negative breast cancer.

MeSH terms

  • A549 Cells
  • Animals
  • Antineoplastic Agents / metabolism*
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Cell Movement / drug effects
  • Cell Movement / immunology
  • Cell Proliferation / drug effects
  • Cell Proliferation / physiology
  • Dose-Response Relationship, Drug
  • Drug Inverse Agonism*
  • ERRalpha Estrogen-Related Receptor
  • Estrogens / metabolism*
  • Estrogens / pharmacology
  • Estrogens / therapeutic use
  • Female
  • Growth Inhibitors / metabolism*
  • Growth Inhibitors / pharmacology
  • Growth Inhibitors / therapeutic use
  • HEK293 Cells
  • HeLa Cells
  • Humans
  • MCF-7 Cells
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Protein Binding / physiology
  • Receptors, Estrogen / metabolism*
  • Triple Negative Breast Neoplasms / drug therapy
  • Triple Negative Breast Neoplasms / metabolism*
  • Xenograft Model Antitumor Assays / methods

Substances

  • Antineoplastic Agents
  • Estrogens
  • Growth Inhibitors
  • Receptors, Estrogen