Smad3 regulates E-cadherin via miRNA-200 pathway (Q39454247)

12 September 2017

Smad3 regulates E-cadherin via miRNA-200 pathway (English)

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12 September 2017

S-M Ahn

1

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12 September 2017

J-Y Cha

2

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12 September 2017

J Kim

3

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12 September 2017

D Kim

4

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12 September 2017

H T H Trang

5

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12 September 2017

Y-M Kim

6

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12 September 2017

Y-H Cho

7

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12 September 2017

D Park

8

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12 September 2017

S Hong

9

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12 September 2017

language of work or name

English

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publication date

24 October 2011

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12 September 2017

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12 September 2017

31

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12 September 2017

3051-3059

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12 September 2017

25

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https://scigraph.springernature.com/pub.10.1038/onc.2011.484

12 September 2017

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The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1

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Loss of the Smad3 expression increases susceptibility to tumorigenicity in human gastric cancer.

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The microRNAs miR-373 and miR-520c promote tumour invasion and metastasis

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The miR-200 family inhibits epithelial-mesenchymal transition and cancer cell migration by direct targeting of E-cadherin transcriptional repressors ZEB1 and ZEB2

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The miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2

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Smad3 is key to TGF-beta-mediated epithelial-to-mesenchymal transition, fibrosis, tumor suppression and metastasis.

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The two faces of transforming growth factor beta in carcinogenesis

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Angiotensin II induces connective tissue growth factor and collagen I expression via transforming growth factor-beta-dependent and -independent Smad pathways: the role of Smad3

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31 March 2020

Identifiers

DOI

10.1038/ONC.2011.484

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Dimensions Publication ID

12 September 2017

1010147130

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Fatcat ID

release_e7jdf73qovhxnesipllc43bj6y

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1 reference