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53BP1 suppresses epithelial-mesenchymal transition by downregulating ZEB1 through microRNA-200b/429 in breast cancer.

Kong X, Ding X, Li X, Gao S, Yang Q - Cancer Sci. (2015)

Bottom Line: Consistently, in MCF-7 breast cancer cells, low 53BP1 expression reduced E-cadherin expression, resulting in increased migration and invasion.These effects were reversed by miR-200b and miR-429 inhibition or overexpression.It was also found that 53BP1 was associated with lymph node metastasis.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Surgery, Qilu Hospital, Shandong University, Jinan, China.

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Related in: MedlinePlus

53BP1 regulated ZEB1 expression and suppressed epithelial–mesenchymal transition in vivo. Immunohistochemistry of 53BP1 and epithelial–mesenchymal transition markers, including E-cadherin, ZEB1, and vimentin, from sections of tumor xenograft mice injected with MDA-MB-231-Control (Con) cells, MDA-MB-231-53BP1 overexpressed cells, MCF-7-shControl (shCon) cells, and MCF-7-sh53BP1 cells. All experiments were carried out at least three times.
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fig05: 53BP1 regulated ZEB1 expression and suppressed epithelial–mesenchymal transition in vivo. Immunohistochemistry of 53BP1 and epithelial–mesenchymal transition markers, including E-cadherin, ZEB1, and vimentin, from sections of tumor xenograft mice injected with MDA-MB-231-Control (Con) cells, MDA-MB-231-53BP1 overexpressed cells, MCF-7-shControl (shCon) cells, and MCF-7-sh53BP1 cells. All experiments were carried out at least three times.

Mentions: Our results were confirmed in vivo in a tumor xenograft mice model conducted previously. Immunohistochemistry analysis of MDA-MB-231-53BP1 tumors showed that ZEB1 and vimentin expression decreased, whereas E-cadherin expression increased. Consistently, ZEB1 and vimentin increased and E-cadherin expression decreased in MCF-7-sh53BP1 tumor sections (Fig.5). Taken together, these data indicated that 53BP1 is a positive regulator of E-cadherin through downregulating the expression of the E-cadherin repressor ZEB1.


53BP1 suppresses epithelial-mesenchymal transition by downregulating ZEB1 through microRNA-200b/429 in breast cancer.

Kong X, Ding X, Li X, Gao S, Yang Q - Cancer Sci. (2015)

53BP1 regulated ZEB1 expression and suppressed epithelial–mesenchymal transition in vivo. Immunohistochemistry of 53BP1 and epithelial–mesenchymal transition markers, including E-cadherin, ZEB1, and vimentin, from sections of tumor xenograft mice injected with MDA-MB-231-Control (Con) cells, MDA-MB-231-53BP1 overexpressed cells, MCF-7-shControl (shCon) cells, and MCF-7-sh53BP1 cells. All experiments were carried out at least three times.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4556386&req=5

fig05: 53BP1 regulated ZEB1 expression and suppressed epithelial–mesenchymal transition in vivo. Immunohistochemistry of 53BP1 and epithelial–mesenchymal transition markers, including E-cadherin, ZEB1, and vimentin, from sections of tumor xenograft mice injected with MDA-MB-231-Control (Con) cells, MDA-MB-231-53BP1 overexpressed cells, MCF-7-shControl (shCon) cells, and MCF-7-sh53BP1 cells. All experiments were carried out at least three times.
Mentions: Our results were confirmed in vivo in a tumor xenograft mice model conducted previously. Immunohistochemistry analysis of MDA-MB-231-53BP1 tumors showed that ZEB1 and vimentin expression decreased, whereas E-cadherin expression increased. Consistently, ZEB1 and vimentin increased and E-cadherin expression decreased in MCF-7-sh53BP1 tumor sections (Fig.5). Taken together, these data indicated that 53BP1 is a positive regulator of E-cadherin through downregulating the expression of the E-cadherin repressor ZEB1.

Bottom Line: Consistently, in MCF-7 breast cancer cells, low 53BP1 expression reduced E-cadherin expression, resulting in increased migration and invasion.These effects were reversed by miR-200b and miR-429 inhibition or overexpression.It was also found that 53BP1 was associated with lymph node metastasis.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Surgery, Qilu Hospital, Shandong University, Jinan, China.

Show MeSH
Related in: MedlinePlus