June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
The effects of acetylsalicylic acid as an anti-tumor agent in a metastatic ocular melanoma cell line
Author Affiliations & Notes
  • Dominique Fausto de Souza
    The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, QC, Canada
  • Sultan Aldrees
    The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, QC, Canada
  • Mohammed F Qutub
    The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, QC, Canada
  • Sarah Alghamdi
    The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, QC, Canada
  • Ana Beatriz Toledo Dias
    The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, QC, Canada
  • Miguel N Burnier
    The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, QC, Canada
  • Footnotes
    Commercial Relationships Dominique Fausto de Souza, None; Sultan Aldrees, None; Mohammed Qutub, None; Sarah Alghamdi, None; Ana Beatriz Dias, None; Miguel Burnier, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 5336. doi:
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      Dominique Fausto de Souza, Sultan Aldrees, Mohammed F Qutub, Sarah Alghamdi, Ana Beatriz Toledo Dias, Miguel N Burnier; The effects of acetylsalicylic acid as an anti-tumor agent in a metastatic ocular melanoma cell line. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5336.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Acetylsalicylic acid (ASA) was shown to inhibit proliferation, angiogenesis and induce apoptosis in colorectal, ovarian and endometrial cancer cells. Moreover, ASA has been shown to abrogate various processes that contribute to tumor growth and progression, via both COX-2 dependent and independent mechanisms. Currently, ASA is being evaluated in clinical trials as an adjuvant therapy to treat multiple cancer types. The goal of the current study is to evaluate the effects of ASA on metastatic uveal melanoma (UM) cells.

Methods: OMM1.5, a well characterized UM cell line derived from a metastatic liver nodule, was used in the current study. OMM1.5 cells were treated with 5 mM ASA for 48 hours and compared to their untreated counterparts for their ability to secrete a panel of 10 proangiogenic cytokines using a sandwich ELISA-based array. Additionally, the functional characteristics of treated and untreated cells were compared using proliferation, invasion, and migration assays.

Results: Treatment with ASA caused a significant decrease in angiogenin and PIGF secretion, and an increase in HB-EGF secretion (P<0.05). No significant change was seen for the other seven proangiogenic cytokines, which included ANG-2, EGF, bFGF, HGF, Leptin, PDGF-BB, and VEGF. Moreover, treatment with ASA significantly inhibited the proliferation and invasion capabilities of OMM1.5 cells (P<0.05 for both).

Conclusions: These results suggest that ASA may be effective as an adjuvant therapy to reduce the proliferation and invasion of metastatic UM. Future studies are needed to determine the mechanisms underlying how ASA simultaneously increase and decreases some proangiogenic cytokines in metastatic UM cell lines.

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