Publications by authors named "Kushlani Gunawardena"

Background: Androgens, while essential for prostate gland development, have been postulated to contribute to carcinogenesis, and antioxidants have been postulated to suppress prostate cancer development. We theorized that antioxidants might suppress prostate cancer cell growth by blocking androgen effects on cell survival. This hypothesis was tested by in vitro studies conducted in ALVA-101, an androgen responsive human prostate cancer cell line.

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Background: We postulated that combinations of C and E vitamins modulate the antioxidant network and blocks survivin gene expression in androgen-responsive and non-responsive human prostate cancer cell (HPCC) lines.

Methods: ALVA-101 and DU-145 cell growth and apoptosis were estimated using the Cell Titer 96 AQ and cell death detection ELISA. Reverse transcription-polymerase chain reaction, Western blot and electrophoretic mobility shift assay were used to quantify survivin mRNA, protein, nuclear factor kappa B (NF-kappaB), and activator protein-1 (AP-1).

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Transforming growth factor beta-1 (TGFbeta-1) and tumor necrosis factor alpha (TNF-alpha), an activator of nuclear factor kappa B (NF-kappaB), modulate apoptosis and/or cell growth. This study was designed to investigate the activity of NF-kappaB and its regulation of inhibitor of apoptosis gene (c-IAP2) in two human prostate cancer cell lines, DU-145 (which is androgen unresponsive) and ALVA-101 (which is moderately androgen responsive). These cells were treated with and without various concentrations of a strong antioxidant, pyrrolidinedithiocarbamate (PDTC), and TNF-alpha at various time intervals.

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We have investigated the effect of antioxidant-induced apoptosis in human prostate cancer cell lines that is augmented by testosterone (T). In this study, DU-145 (androgen unresponsive), ALVA-101 (partially androgen responsive), and LNCaP (androgen responsive) were grown in tissue culture with RPMI 1640 medium, 5-10% fetal bovine serum (FBS), antibiotics and 5% CO2. Treatment with 2.

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