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Glabridin attenuates the migratory and invasive capacity of breast cancer cells by activating microRNA-200c.

Ye X, Jiang F, Li Y, Mu J, Si L, Wang X, Ning S, Li Z - Cancer Sci. (2014)

Bottom Line: However, little is known regarding the effect of microRNA (miRNA) on GLA's anti-metastatic activity.GLA induced the mesenchymal-epithelial transition in vitro and in vivo, as determined by increased expression of the epithelial marker, E-cadherin, and decreased expression of the mesenchymal marker, vimentin.Overexpression of miR-200c enhanced the expression of E-cadherin and decreased the expression of vimentin.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Modern Toxicology, Ministry of Education, Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, China.

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miR-200c is involved in expression of epithelial–mesenchymal transition markers in glabridin (GLA)-treated human breast cancer cells. After MDA-MB-231cells were transfected by con-mimic or miR-200c-mimic for 12 h. (a) quantitative RT-PCR analysis of mir-200c, (b) western blot analyses of E-cadherin and (c) morphological images of MDA-MB-231 cells exposed to con-mimic or miR-200c-mimic. After MDA-MB-231 and BT-549 cells were transfected with anti-con or anti-miR-200c for 12 h, they were exposed to 0 or 10 μM GLA for 48 h. (d) Western blot analyses and (e) relative protein levels of E-cadherin (mean ± SD, n = 3). **P < 0.01 compared with medium control MDA-MB-231 or BT-549 cells, ##P < 0.01 compared with anti-con-transfected MDA-MB-231 or BT-549cells cells exposed to 10 μM GLA.
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fig06: miR-200c is involved in expression of epithelial–mesenchymal transition markers in glabridin (GLA)-treated human breast cancer cells. After MDA-MB-231cells were transfected by con-mimic or miR-200c-mimic for 12 h. (a) quantitative RT-PCR analysis of mir-200c, (b) western blot analyses of E-cadherin and (c) morphological images of MDA-MB-231 cells exposed to con-mimic or miR-200c-mimic. After MDA-MB-231 and BT-549 cells were transfected with anti-con or anti-miR-200c for 12 h, they were exposed to 0 or 10 μM GLA for 48 h. (d) Western blot analyses and (e) relative protein levels of E-cadherin (mean ± SD, n = 3). **P < 0.01 compared with medium control MDA-MB-231 or BT-549 cells, ##P < 0.01 compared with anti-con-transfected MDA-MB-231 or BT-549cells cells exposed to 10 μM GLA.

Mentions: miR-200c is involved in regulating the EMT.(17) After transfection by con-mimic or miR-200c-mimic for 12 h, overexpression of miR-200c (Fig. 6a) enhanced the expression of E-cadherin in MDA-MB-231 cells (Fig. 6b), which showed an epithelial-like morphology (Fig. 6c). The functions of miR-200c in GLA-mediated mesenchymal–epithelial transition (MET) were determined. After MDA-MB-231 and BT-549 cells were transfected by anti-con or anti-miR-200c for 12 h, they were exposed to 0.0 or 10.0 μM GLA for 2 days. Knockdown of miR-200c reduced the GLA-induced increased expression of E-cadherin (Fig. 6d,e). Meanwhile, knockdown of miR-200a mildly reduced the GLA-induced increased expression of E-cadherin (Fig. S1a,b).


Glabridin attenuates the migratory and invasive capacity of breast cancer cells by activating microRNA-200c.

Ye X, Jiang F, Li Y, Mu J, Si L, Wang X, Ning S, Li Z - Cancer Sci. (2014)

miR-200c is involved in expression of epithelial–mesenchymal transition markers in glabridin (GLA)-treated human breast cancer cells. After MDA-MB-231cells were transfected by con-mimic or miR-200c-mimic for 12 h. (a) quantitative RT-PCR analysis of mir-200c, (b) western blot analyses of E-cadherin and (c) morphological images of MDA-MB-231 cells exposed to con-mimic or miR-200c-mimic. After MDA-MB-231 and BT-549 cells were transfected with anti-con or anti-miR-200c for 12 h, they were exposed to 0 or 10 μM GLA for 48 h. (d) Western blot analyses and (e) relative protein levels of E-cadherin (mean ± SD, n = 3). **P < 0.01 compared with medium control MDA-MB-231 or BT-549 cells, ##P < 0.01 compared with anti-con-transfected MDA-MB-231 or BT-549cells cells exposed to 10 μM GLA.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig06: miR-200c is involved in expression of epithelial–mesenchymal transition markers in glabridin (GLA)-treated human breast cancer cells. After MDA-MB-231cells were transfected by con-mimic or miR-200c-mimic for 12 h. (a) quantitative RT-PCR analysis of mir-200c, (b) western blot analyses of E-cadherin and (c) morphological images of MDA-MB-231 cells exposed to con-mimic or miR-200c-mimic. After MDA-MB-231 and BT-549 cells were transfected with anti-con or anti-miR-200c for 12 h, they were exposed to 0 or 10 μM GLA for 48 h. (d) Western blot analyses and (e) relative protein levels of E-cadherin (mean ± SD, n = 3). **P < 0.01 compared with medium control MDA-MB-231 or BT-549 cells, ##P < 0.01 compared with anti-con-transfected MDA-MB-231 or BT-549cells cells exposed to 10 μM GLA.
Mentions: miR-200c is involved in regulating the EMT.(17) After transfection by con-mimic or miR-200c-mimic for 12 h, overexpression of miR-200c (Fig. 6a) enhanced the expression of E-cadherin in MDA-MB-231 cells (Fig. 6b), which showed an epithelial-like morphology (Fig. 6c). The functions of miR-200c in GLA-mediated mesenchymal–epithelial transition (MET) were determined. After MDA-MB-231 and BT-549 cells were transfected by anti-con or anti-miR-200c for 12 h, they were exposed to 0.0 or 10.0 μM GLA for 2 days. Knockdown of miR-200c reduced the GLA-induced increased expression of E-cadherin (Fig. 6d,e). Meanwhile, knockdown of miR-200a mildly reduced the GLA-induced increased expression of E-cadherin (Fig. S1a,b).

Bottom Line: However, little is known regarding the effect of microRNA (miRNA) on GLA's anti-metastatic activity.GLA induced the mesenchymal-epithelial transition in vitro and in vivo, as determined by increased expression of the epithelial marker, E-cadherin, and decreased expression of the mesenchymal marker, vimentin.Overexpression of miR-200c enhanced the expression of E-cadherin and decreased the expression of vimentin.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Modern Toxicology, Ministry of Education, Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, China.

Show MeSH
Related in: MedlinePlus