Abdul Hamid, Auni Fatin
(2016)
Effects Of Oxidized Low-Density Lipoprotein By Thymoquinone In Lipidloaded Mcf-7 Breast Cancer Cells.
Masters thesis, Universiti Sains Malaysia.
Abstract
Kanser payudara adalah punca utama kematian di kalangan wanita di seluruh
dunia dan kajian baru-baru ini mendedahkan bahawa lipoprotein berketumpatan
rendah teroksida (ox-LDL) menyumbang kepada peningkatan risiko kanser payudara.
Thymoquinone (TQ) telah dikaji secara meluas dalam patogenesis kanser melalui in
vivo dan in vitro, tetapi terdapat kekurangan laporan mengenai kawal atur lipid dalam
sel kanser. Oleh itu, objektif kajian ini adalah untuk menjelaskan kesan ox-LDL
kepada pertumbuhan sel kanser payudara serta mekanisma metabolisma lipid dan
pertumbuhan sel di peringkat molekul yang dikawal atur oleh TQ. Kesan toksik TQ
dianalisis melalui ujian MTS. Sel MCF-7 didedahkan kepada 10 μg/ml ox-LDL,
diikuti oleh rawatan dengan 20 μM TQ untuk kajian ke atas kebergantungan kepada
masa. Lokasi dan ekspresi protein sasaran dikaji melalui kaedah immunopendarfluor
dan pemendapan Western. Ini diikuti oleh analisis qRT-PCR ke atas ekspresi VAMP4
dan EGLN1.
Breast cancer is the leading cause of death among women worldwide and
recent studies revealed that oxidized low-density lipoprotein (ox-LDL) contributed to
increased risk of breast cancer. To date, thymoquinone (TQ) is widely studied both in
vivo and in vitro in cancer pathogenesis, but there is lack of reports on its lipid
regulation in cancer cells. Thus, the objectives of this study were to elucidate the
effects of ox-LDL on breast cancer cell growth as well as the molecular mechanisms
of lipid metabolism and cell proliferation regulated by TQ. Cytotoxicity of TQ was
analyzed using MTS assay. MCF-7 cells were exposed to 10 μg/ml of ox-LDL,
followed by treatment with 20 μM of TQ for time-dependent study. Localization and
expression of target proteins were studied through immunofluorescence and Western
blot methods. This was followed by qRT-PCR analysis on genomic expression of
VAMP4 and EGLN1.
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