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Implantation and Evaluation of Melanoma in the Murine Choroid via Optical Coherence Tomography
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Uveal Melanoma Cell Line Proliferation Is Inhibited by Ricolinostat, a Histone Deacetylase Inhibitor.

Husvinee Sundaramurthi1,2,3,4, Sandra García-Mulero5,6, Valentina Tonelotto1,2,7

  • 1UCD Conway Institute, University College Dublin, D04 V1W8 Dublin, Ireland.

Cancers
|February 15, 2022
PubMed
Summary

ACY-1215, a histone deacetylase inhibitor (HDACi), effectively reduces uveal melanoma cell growth and survival. This HDAC inhibitor shows promise in attenuating metastatic uveal melanoma (MUM) by targeting the MITF pathway.

Keywords:
ACY-1215HDAC inhibitorMITFML329metastatic uveal melanomap-ERKzebrafish xenografts

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Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Metastatic uveal melanoma (MUM) presents a significant clinical challenge with limited effective treatments.
  • Current therapeutic strategies for MUM offer minimal patient survival benefits, necessitating novel approaches.

Purpose of the Study:

  • To evaluate the efficacy of ACY-1215, a histone deacetylase inhibitor (HDACi), against ocular and liver metastatic uveal melanoma (MUM) cell lines.
  • To elucidate the molecular mechanisms underlying the anti-cancer effects of ACY-1215, focusing on cell cycle, apoptosis, and signaling pathways.

Main Methods:

  • In vitro and in vivo studies using primary ocular UM cell lines (Mel270) and a liver MUM cell line (OMM2.5).
  • Assessment of cell survival, proliferation, cell cycle arrest (flow cytometry), apoptosis, and protein expression (p-ERK).
  • Proteome profiling to identify affected signaling pathways, including microphthalmia-associated transcription factor (MITF), and validation with ML329.

Main Results:

  • ACY-1215 demonstrated a significant, dose-dependent reduction in the survival of Mel270 and OMM2.5 cells in vitro.
  • In vivo studies showed ACY-1215 attenuated OMM2.5 xenografts in zebrafish larvae.
  • ACY-1215 induced S-phase cell cycle arrest and apoptosis in OMM2.5 cells, reducing p-ERK levels and impacting MITF signaling.

Conclusions:

  • ACY-1215 exhibits significant anti-cancer activity against uveal melanoma cells, both in vitro and in vivo.
  • The anti-cancer effects are mediated through cell cycle arrest, apoptosis induction, and modulation of the MITF signaling pathway.
  • ACY-1215 and MITF inhibition with ML329 represent potential therapeutic strategies for metastatic uveal melanoma.