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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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Glabridin (GLA) enhances the expression of miR-200s in MDA-MB-231 and BT-549 cells. MDA-MB-231 (a) and BT-549 (b) cells were exposed to 10 μM GLA for 48 h. Quantitative RT-PCR analysis of their miR-200a, miR-200b, miR-200c, miR-141 and miR-429. *P < 0.05 and **P < 0.01 compared with medium control MDA-MB-231 and BT-549 cells.
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fig05: Glabridin (GLA) enhances the expression of miR-200s in MDA-MB-231 and BT-549 cells. MDA-MB-231 (a) and BT-549 (b) cells were exposed to 10 μM GLA for 48 h. Quantitative RT-PCR analysis of their miR-200a, miR-200b, miR-200c, miR-141 and miR-429. *P < 0.05 and **P < 0.01 compared with medium control MDA-MB-231 and BT-549 cells.

Mentions: miR-200s are involved in regulating the EMT and cancer cell invasion through inhibition of the E-cadherin transcriptional repressors, ZEB1/2.(18) Here, in MDA-MB-231 cells exposed to GLA, there were increased expressions of miR-200a, miR-200c and miR-141 (Fig. 5a). For BT-549 cells, GLA elevated all miR-200s tested, except miR-429 (Fig. 5b). For both types of cells, GLA upregulated the expression of miR-200c more extensively. Moreover, GLA elevated the expressions of miR-200a, miR-200b, miR-200c, miR-141 and miR-429 in tumors formed by MDA-MB-231 cells (Fig. 4d).


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)

Glabridin (GLA) enhances the expression of miR-200s in MDA-MB-231 and BT-549 cells. MDA-MB-231 (a) and BT-549 (b) cells were exposed to 10 μM GLA for 48 h. Quantitative RT-PCR analysis of their miR-200a, miR-200b, miR-200c, miR-141 and miR-429. *P < 0.05 and **P < 0.01 compared with medium control MDA-MB-231 and BT-549 cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317926&req=5

fig05: Glabridin (GLA) enhances the expression of miR-200s in MDA-MB-231 and BT-549 cells. MDA-MB-231 (a) and BT-549 (b) cells were exposed to 10 μM GLA for 48 h. Quantitative RT-PCR analysis of their miR-200a, miR-200b, miR-200c, miR-141 and miR-429. *P < 0.05 and **P < 0.01 compared with medium control MDA-MB-231 and BT-549 cells.
Mentions: miR-200s are involved in regulating the EMT and cancer cell invasion through inhibition of the E-cadherin transcriptional repressors, ZEB1/2.(18) Here, in MDA-MB-231 cells exposed to GLA, there were increased expressions of miR-200a, miR-200c and miR-141 (Fig. 5a). For BT-549 cells, GLA elevated all miR-200s tested, except miR-429 (Fig. 5b). For both types of cells, GLA upregulated the expression of miR-200c more extensively. Moreover, GLA elevated the expressions of miR-200a, miR-200b, miR-200c, miR-141 and miR-429 in tumors formed by MDA-MB-231 cells (Fig. 4d).

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