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MicroRNA-137 inhibits BMP7 to enhance the epithelial-mesenchymal transition of breast cancer cells

View Article: PubMed Central - PubMed

ABSTRACT

Bone morphogenetic protein-7 (BMP7) is known to antagonize transforming growth factor β 1 (TGFβ1)-mediated fibrosis through suppressing epithelial-mesenchymal transition (EMT). We recently reported that BMP7 also antagonizes the effects of TGFβ1 in breast cancer (BC) tumorigenesis-related EMT. Nevertheless, the control of BMP7 expression in BC remains ill-defined. Here, we detected significantly lower levels of BMP7 and significantly higher levels of microRNA-137 (miR-137) in the BC specimens, relative to paired adjacent non-tumor breast tissue. BMP7 and miR-137 levels were correlated inversely. Additionally, the high miR-137 levels in BC specimens were correlated with reduced patient survival. In vitro, overexpression of miR-137 significantly increased cell EMT and invasion, while depletion of miR-137 significantly decreased cell EMT and invasion in BC cells. The increases in BC cell invasiveness by miR-137 appeared to result from its suppression of BMP7, through direct binding of miR-137 to the 3'-UTR of BMP7 mRNA, thereby blocking its protein translation in BC cells. This study sheds light on miR-137 as a crucial factor that enhances BC cell EMT and invasiveness, and points to miR-137 as a promising innovative therapeutic target for BC treatment.

No MeSH data available.


MiR-137 decreases BMP7 protein but not mRNA in BC cellsA-B. The BMP7 levels in miR-137-overexpressing (and BMP7-overexpressing) MCF7 cells by RT-qPCR (A) and by Western blot (B). C-D. The BMP7 levels in miR-137-depleted (and BMP7-depleted) BT474 cells by RT-qPCR (C) and by Western blot (D). *p<0.05. NS: non-significant. N=5.
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Figure 3: MiR-137 decreases BMP7 protein but not mRNA in BC cellsA-B. The BMP7 levels in miR-137-overexpressing (and BMP7-overexpressing) MCF7 cells by RT-qPCR (A) and by Western blot (B). C-D. The BMP7 levels in miR-137-depleted (and BMP7-depleted) BT474 cells by RT-qPCR (C) and by Western blot (D). *p<0.05. NS: non-significant. N=5.

Mentions: The effects of miR-137 on BMP7 were then examined in BC cells. The BMP7 mRNA did not alter (Figure 3A), but the BMP7 protein was significantly decreased in miR-137-overexpressing MCF7 cells (Figure 3B). Moreover, the BMP7 mRNA did not alter (Figure 3C), but the BMP7 protein was significantly increased in miR-137-depleted BT474 cells (Figure 3D).


MicroRNA-137 inhibits BMP7 to enhance the epithelial-mesenchymal transition of breast cancer cells
MiR-137 decreases BMP7 protein but not mRNA in BC cellsA-B. The BMP7 levels in miR-137-overexpressing (and BMP7-overexpressing) MCF7 cells by RT-qPCR (A) and by Western blot (B). C-D. The BMP7 levels in miR-137-depleted (and BMP7-depleted) BT474 cells by RT-qPCR (C) and by Western blot (D). *p<0.05. NS: non-significant. N=5.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5392333&req=5

Figure 3: MiR-137 decreases BMP7 protein but not mRNA in BC cellsA-B. The BMP7 levels in miR-137-overexpressing (and BMP7-overexpressing) MCF7 cells by RT-qPCR (A) and by Western blot (B). C-D. The BMP7 levels in miR-137-depleted (and BMP7-depleted) BT474 cells by RT-qPCR (C) and by Western blot (D). *p<0.05. NS: non-significant. N=5.
Mentions: The effects of miR-137 on BMP7 were then examined in BC cells. The BMP7 mRNA did not alter (Figure 3A), but the BMP7 protein was significantly decreased in miR-137-overexpressing MCF7 cells (Figure 3B). Moreover, the BMP7 mRNA did not alter (Figure 3C), but the BMP7 protein was significantly increased in miR-137-depleted BT474 cells (Figure 3D).

View Article: PubMed Central - PubMed

ABSTRACT

Bone morphogenetic protein-7 (BMP7) is known to antagonize transforming growth factor &beta; 1 (TGF&beta;1)-mediated fibrosis through suppressing epithelial-mesenchymal transition (EMT). We recently reported that BMP7 also antagonizes the effects of TGF&beta;1 in breast cancer (BC) tumorigenesis-related EMT. Nevertheless, the control of BMP7 expression in BC remains ill-defined. Here, we detected significantly lower levels of BMP7 and significantly higher levels of microRNA-137 (miR-137) in the BC specimens, relative to paired adjacent non-tumor breast tissue. BMP7 and miR-137 levels were correlated inversely. Additionally, the high miR-137 levels in BC specimens were correlated with reduced patient survival. In vitro, overexpression of miR-137 significantly increased cell EMT and invasion, while depletion of miR-137 significantly decreased cell EMT and invasion in BC cells. The increases in BC cell invasiveness by miR-137 appeared to result from its suppression of BMP7, through direct binding of miR-137 to the 3'-UTR of BMP7 mRNA, thereby blocking its protein translation in BC cells. This study sheds light on miR-137 as a crucial factor that enhances BC cell EMT and invasiveness, and points to miR-137 as a promising innovative therapeutic target for BC treatment.

No MeSH data available.