Premium
Anti‐Cancer Effect of Fluorinated Caffeic Acid Phenethyl Ester on Multiple Myeloma Cells
Author(s) -
Marin Elizabeth Hernandez,
Wang Xinyu
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb533
Subject(s) - caffeic acid phenethyl ester , apoptosis , multiple myeloma , oxidative stress , caffeic acid , cancer research , flow cytometry , cytotoxicity , programmed cell death , pharmacology , chemistry , medicine , biochemistry , antioxidant , immunology , in vitro
Multiple myeloma (MM) is a plasma cell malignancy that occurs in the bone marrow. It is responsible for approximately 1% of all cancer related deaths and remains as an incurable disease. Recently, polyphenolic compounds have demonstrated therapeutic potential in treating various cancers, including hematological cancers. Our preliminary data has shown that Caffeic acid phenethyl ester (CAPE), a polyphenolic compound found in bee propolis, can inhibit MM cell growth and cause cell death through apoptosis. In addition, it suggests that oxidative stress could be responsible for initiating apoptosis. Fluorinated caffeic acid phenethyl ester (F‐CAPE), a novel derivative of CAPE that was previously synthesized in our lab, could potentially serve as an effective multiple myeloma treatment. Because F‐CAPE was found to be more stable that CAPE in rat plasma, it could be a better candidate for multiple myeloma treatment than its parental compound. We hypothesize that F‐CAPE induces apoptosis in MM cells through oxidative stress. We observed a time and dose dependent decrease in MM cell growth following F‐CAPE treatment. Our data showed that F‐CAPE is more potent than its parental CAPE. Our flow cytometry data suggest that F‐CAPE induced apoptosis in treated MM cells to a greater extent than CAPE. Western blot imaging of various pro and anti‐apoptotic proteins such as Bax, Bak and Bcl‐2, confirmed the role of apoptosis in MM cell death. Preliminary experiments with the antioxidant, N‐acetyl cysteine, have shown to ameliorate the cytotoxicity effect of F‐CAPE in MM cells. This suggests that the production of oxidative stress could be the mechanism through which F‐CAPE causes apoptosis in multiple myeloma cells. Support or Funding Information Philadelphia College of Osteopathic Medicine CRSO Intramural FundingViability of MM RPMI 8226 cells after FCAPE treatment. Cells were plated in a 48 well plate (40,000 cells/ well) and allowed to incubate for 24,48 and 72 hours following FCAPE treatment (1~50 μM). The present data indicates a time and dose dependent decrease after FCAPE treatment.