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发布于:2019-1-20 11:15:22  访问:9 次 回复:0 篇
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Eously observed that an increase in cell migration was accompanied with
(B) LoVo cells cultured in DMEM have been treated with PGE2 (10-6M) for numerous periods (15 min, 30 min, 1 h, 3 h, six h, 12 h and 24 h), and Tubacin web subsequently measured the phosphorylation/activation of proteins by immunoblotting assay. Journal of Biomedical Science 2011, 18:61 http://www.jbiomedsci.com/content/18/1/Page 7 ofFigure 4 17b-Estradiol down-regulates PGE2-induced uPA and MMP-9 expression by suppressing activation of JNK1/2 in human LoVo cells. (A) LoVo cells cultured in DMEM were treated with 17b-estradiol (10-8M) for various periods (5 min, 15 min, 30 min, 1 h, 3 h, 6 h, 12 h and 24 h), and subsequently measured the phosphorylation/activation of proteins by immunoblotting assay. The fold ratio of p-JNK1/2 and JNK1/2 was measured. (B) LoVo cells were pretreated with 17b-estradiol (10-8M) for 30 min, followed by PGE2 (10-6M) treatment for 30 min or 24 h, and then were subjected to immunoblotting assay for protein detection of phospho-JNK1/2 (PGE2 stimulation within 30 min); uPA and MMP9 (PGE2 stimulation within 24 h).expression by suppressing activation of JNK1/2. PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26437915 These final results demonstrate that 17b-estradiol may perhaps efficiently inhibit PGE2-induced motility in human LoVo colon cancer cells (Figure 6). Upregulation of MMPs is reported to contribute to ECM remodeling, tumor cell invasion and metastasis, as a result major towards the improvement of malignant tumor [5]. Each mRNA levels MMP-2 and MMP-9 have been located to be overexpressed in colon carcinomas [21,22]. Within the observations of Collins et al. [23], MMP-2 mRNA is additional substantially expressed in tumor lesions than in typical colon tissues. Immunostaining assay showed that MMP-9 expression is much more frequently present in advanced tumor stages, and in invasive tumor regions wherein cancer cellsare in close proximity of inflammatory cells, suggesting that locally proteolytic and collagenlytic activities contributes to the property of invasion in colorectal cancers [24].Eously observed that a rise in cell migration was accompanied with all the upregulation of migration-related things which includes uPA and MMP-9, following PGE2 (10-6M) treatment. Moreover, JNK1/2 mediated PGE2-induced expression of uPA and MMP-9 in LoVo cells. (three) However, PGE2 (ten -6 M) treatment showed no influences on regulating the expression of PAI-1, TIMP-1, TIMP-2, TIMP-3 and TIMP-4 in LoVo cells. (four) PGE2-induced expression of uPA and MMP-9 in human LoVo cells was drastically inhibited by 17bestradiol (ten -8 M) pretreatment. 17b-Estradiol drastically inhibited PGE2-induced uPA and MMP-Hsu et al. Journal of Biomedical Science 2011, 18:61 http://www.jbiomedsci.com/content/18/1/Page 6 ofFigure three PGE2 upregulates uPA and MMP-9 through JNK1/2 signaling pathway in human LoVo colon cancer cells. (A) LoVo cells were pretreated with vehicle, LY294002 (Akt activation inhibitor), U0126 (ERK1/2 activation inhibitor, 1 M), SB203580 (p38 MAPK inhibitor, 1 M), SP600125 (JNK1/2 inhibitor, 1 M) or QNZ (NFB inhibitor, 1 M) for 1 h and followed by PGE2 (10-6M) administration for 24 h, after which have been harvested for immunoblotting assays.
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