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  1. Indah M Amin, Mohd Ridzuan Hamid, Dayang Zahidah A. Othman, Rosfaiizah Siran, Siti Hamimah S.A. Kadir, Narimah AH Hasani
    ASM Science Journal, 2014;8(2):165-173.
    MyJurnal
    Aloe emodin, an anthraquinone of Aloe barbadensis Miller has been shown to have more cytotoxic effect in
    different kinds of human cancer cell lines compared to normal. Accordingly, we found it to selectively inhibit
    the proliferation of oestrogen-receptor-positive-(ER+)-breast cancer cells, MCF-7; but not controls cells,
    MCF-10A. However, its precise mechanism is not well understood. Several studies have shown that there is
    evidence of increased intracellular calcium (Ca2+), both at early and late stage of apoptosis which associated
    with the down-regulation of ERK1/2 proliferative pathway. Therefore, we aim to elucidate the involvement
    of intracellular Ca2+ in aloe emodin induced apoptosis on MCF-7. Apoptotic morphological changes were
    observed under fluorescence microscope. The involvement of cytoplasmic Ca2+ and MAPKs were investigated
    using Fluo-4 intracellular Ca2+ imaging and QuantiGene 2.0 Plex assay, respectively. IC50 of aloe emodin
    (80 μM) at 72 hours incubation was used. Data were evaluated using the one-way or two-way ANOVA tests.
    Our results indicated that aloe emodin at IC50 80µM induced apoptosis on MCF-7 through the association of
    intracellular Ca2+ signalling. This observation include a significant increased (p
  2. Narimah Abdul Hamid Hasani, Siti Hamimah Sheikh Abdul Kadir, Indah Mohd Amin, Roziana Kamaludin, Rosfaiizah Siran, Mohamad Rodi Isa, et al.
    Sains Malaysiana, 2015;44:1137-1143.
    Two-third of breast cancer patients expressed estrogen receptors (ER)s and received endocrine treatment with established anti-estrogens such as tamoxifen. But the action and acquired resistance during treatment are largely unknown. In contrary, phytochemicals are more selective and less cytotoxic to normal cells. Accordingly, we found aloe emodin, an anthraquinone to inhibit the proliferation of ER+-breast cancer cells, MCF-7 with IC50 of 80 µM, but not affecting control breast cells, MCF-10A. Tamoxifen was non-selective to both cells with IC50 of 27 and 38 μM, respectively. Thus, we aimed to investigate the anti-proliferative mechanism of aloe emodin on MCF-7 and its underlying signalling compared to tamoxifen. Cells were treated separately with aloe emodin and tamoxifen at respective IC50 for 72 h. Apoptosis was determined using Annexin V-FITC/PI staining. The expression of insulin-like growth factor-1 receptor (IGF-1R), insulin like growth factor binding protein (IGFBP)-2 and B-raf gene was investigated using QuantiGene 2.0 Plex assay. Pairedstudent t-test and ANOVA test were used to compare between untreated and treated cells on the measured parameters. Each treatment was conducted in triplicate and repeated three times. Significance was set at p<0.05. The presences of early and late apoptosis in MCF-7 were seen in both treatments. All target genes were down regulated. The anti-proliferation effect of aloe emodin on MCF-7 is similar with tamoxifen which mediates inhibition of IGF-1R signalling pathway. This suggests aloe emodin as a potential anti-cancer agent to be used in combined anti-estrogen therapy to enhance its efficacy in ER+-breast cancer treatment.
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