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[Effects of tamoxifen on apoptosis and matrix metalloproteinase-7 expression in estrogen receptor beta-positive colonic cancer cell line HT-29].

Yu-Jing Fang, Guo-Qiang Wang, Zhen Lü, Li Yi Zhang, Zhi Zhong Pan, Zhi Zhou, De Sen Wan

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Abstract

BACKGROUND & OBJECTIVE: Studies have shown that estrogen receptor beta (ERbeta), which is highly expressed in colorectal cancer, is related to tumor metastasis. Matrix metalloproteinase (MMP)-7 is overexpressed in colorectal cancer, and plays an important role in tumor invasion and metastasis. This study was to explore the effect of tamoxifen (TAM) on apoptosis and MMP-7 expression in ERbeta-positive human colorectal cancer cell line HT-29. METHODS: After exposure to TAM, the proliferation of HT-29 cells was detected by MTT assay; cell apoptosis was evaluated using flow cytometry; expressions of ERbeta and MMP-7 were measured by Western blot. RESULTS: TAM significantly inhibited cell growth of HT-29 in a time (24 h, 48 h, 72 h )-and dose (0, 10(-7), 10(-6), 10(-5),0 10(-4) mol/L )-dependent manner. TAM exposure caused significant cell apoptosis of HT-29 cells at the concentration of 10(-4) mol/L [(69.9+/-4.2)%]. Moreover, TAM could bind to ERbeta to down-regulate MMP-7 protein expression in HT-29 cells. CONCLUSION: High concentration of TAM can inhibit the proliferation of ERbeta-positive HT-29 cells, and effectively bind with ERbeta to down-regulate MMP-7 expression.

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BACKGROUND & OBJECTIVE: Studies have shown that estrogen receptor beta (ERbeta), which is highly expressed in colorectal cancer, is related to tumor metastasis. Matrix metalloproteinase (MMP)-7 is overexpressed in colorectal cancer, and plays an important role in tumor invasion and metastasis. This study was to explore the effect of tamoxifen (TAM) on apoptosis and MMP-7 expression in ERbeta-positive human colorectal cancer cell line HT-29. METHODS: After exposure to TAM, the proliferation of HT-29 cells was detected by MTT assay; cell apoptosis was evaluated using flow cytometry; expressions of ERbeta and MMP-7 were measured by Western blot. RESULTS: TAM significantly inhibited cell growth of HT-29 in a time (24 h, 48 h, 72 h )-and dose (0, 10(-7), 10(-6), 10(-5),0 10(-4) mol/L )-dependent manner. TAM exposure caused significant cell apoptosis of HT-29 cells at the concentration of 10(-4) mol/L [(69.9+/-4.2)%]. Moreover, TAM could bind to ERbeta to down-regulate MMP-7 protein expression in HT-29 cells. CONCLUSION: High concentration of TAM can inhibit the proliferation of ERbeta-positive HT-29 cells, and effectively bind with ERbeta to down-regulate MMP-7 expression.

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Available abstract

BACKGROUND & OBJECTIVE: Studies have shown that estrogen receptor beta (ERbeta), which is highly expressed in colorectal cancer, is related to tumor metastasis. Matrix metalloproteinase (MMP)-7 is overexpressed in colorectal cancer, and plays an important role in tumor invasion and metastasis. This study was to explore the effect of tamoxifen (TAM) on apoptosis and MMP-7 expression in ERbeta-positive human colorectal cancer cell line HT-29. METHODS: After exposure to TAM, the proliferation of HT-29 cells was detected by MTT assay; cell apoptosis was evaluated using flow cytometry; expressions of ERbeta and MMP-7 were measured by Western blot. RESULTS: TAM significantly inhibited cell growth of HT-29 in a time (24 h, 48 h, 72 h )-and dose (0, 10(-7), 10(-6), 10(-5),0 10(-4) mol/L )-dependent manner. TAM exposure caused significant cell apoptosis of HT-29 cells at the concentration of 10(-4) mol/L [(69.9+/-4.2)%]. Moreover, TAM could bind to ERbeta to down-regulate MMP-7 protein expression in HT-29 cells. CONCLUSION: High concentration of TAM can inhibit the proliferation of ERbeta-positive HT-29 cells, and effectively bind with ERbeta to down-regulate MMP-7 expression.

Key concepts: Apoptosis, Estrogen receptor, Cancer research, Flow cytometry, Tamoxifen, Downregulation and upregulation, Metastasis, Cell growth

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[Effects of tamoxifen on apoptosis and matrix metalloproteinase-7 expression in estrogen receptor beta-positive colonic cancer cell line HT-29]. — Research Paper | ScholarLens