MicroRNA-376c Impairs Transforming Growth Factor-β and Nodal Signaling to Promote Trophoblast Cell Proliferation and Invasion

Hypertension ◽  
2013 ◽  
Vol 61 (4) ◽  
pp. 864-872 ◽  
Author(s):  
Guodong Fu ◽  
Gang Ye ◽  
Lubna Nadeem ◽  
Lei Ji ◽  
Tanita Manchanda ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Trophoblast Cell ◽  
Nodal Signaling ◽  
Proliferation And Invasion

scholarly journals Suppressive Role of MicroRNA-148a in Cell Proliferation and Invasion in Ovarian Cancer Through Targeting Transforming Growth Factor-β-Induced 2

2016 ◽  
Vol 24 (5) ◽  
pp. 353-360 ◽  
Author(s):  
Min Zhao ◽  
Zhiying Su ◽  
Shiyang Zhang ◽  
Liangjin Zhuang ◽  
Yudi Xie ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Underlying Mechanism ◽  
Protein Levels ◽  
Ovarian Epithelial Cells ◽  
Proliferation And Invasion

Ovarian cancer (OC) is one of the most common gynecological malignancies. MicroRNAs (miRs) play a crucial role in the development and progression of OC, but the underlying mechanism remains largely unclear. Our study investigated the regulatory role of miR-148a in OC cell proliferation and invasion. We found that miR-148a was significantly downregulated in OC tissues compared to their matched adjacent nontumor tissues. In addition, its expression was also reduced in OC cell lines (SKOV3, ES-2, OVCAR, and A2780) compared to normal ovarian epithelial cells. Overexpression of miR-148a caused a significant decrease in OC cell proliferation and invasion, as well as reduced MMP9 protein levels. Transforming growth factor-β-induced 2 (TGFI2) was further identified as a target gene of miR-148a, and its protein expression was downregulated in OC cells after miR-148a overexpression. Restoration of TGFI2 attenuated the suppressive effects of miR-148a on OC cell proliferation and invasion. Moreover, we found that TGFI2 was remarkably upregulated in OC tissues when compared with their matched adjacent nontumor tissues, and observed a reverse correlation between miR-148a and TGFI2 expression in OC tissues. On the basis of these findings, we suggest that miR-148a inhibits OC cell proliferation and invasion partly through inhibition of TGFI2. Therefore, our study highlights the importance of the miR-148a/TGFI2 axis in the malignant progression of OC.

Interaction of the transforming growth factor-β and Notch signaling pathways in the regulation of granulosa cell proliferation

2016 ◽  
Vol 28 (12) ◽  
pp. 1873 ◽  
Author(s):  
Xiao-Feng Sun ◽  
Xing-Hong Sun ◽  
Shun-Feng Cheng ◽  
Jun-Jie Wang ◽  
Yan-Ni Feng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Transcription Factor ◽  
Growth Factor ◽  
Granulosa Cell ◽  
Target Genes ◽  
Transforming Growth Factor ◽  
Notch Pathway ◽  
Transforming Growth Factor Β ◽  
Notch Signalling ◽  
Signalling Pathways

The Notch and transforming growth factor (TGF)-β signalling pathways play an important role in granulosa cell proliferation. However, the mechanisms underlying the cross-talk between these two signalling pathways are unknown. Herein we demonstrated a functional synergism between Notch and TGF-β signalling in the regulation of preantral granulosa cell (PAGC) proliferation. Activation of TGF-β signalling increased hairy/enhancer-of-split related with YRPW motif 2 gene (Hey2) expression (one of the target genes of the Notch pathway) in PAGCs, and suppression of TGF-β signalling by Smad3 knockdown reduced Hey2 expression. Inhibition of the proliferation of PAGCs by N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butylester (DAPT), an inhibitor of Notch signalling, was rescued by both the addition of ActA and overexpression of Smad3, indicating an interaction between the TGF-β and Notch signalling pathways. Co-immunoprecipitation (CoIP) and chromatin immunoprecipitation (ChIP) assays were performed to identify the point of interaction between the two signalling pathways. CoIP showed direct protein–protein interaction between Smad3 and Notch2 intracellular domain (NICD2), whereas ChIP showed that Smad3 could be recruited to the promoter regions of Notch target genes as a transcription factor. Therefore, the findings of the present study support the idea that nuclear Smad3 protein can integrate with NICD2 to form a complex that acts as a transcription factor to bind specific DNA motifs in Notch target genes, such as Hey1 and Hey2, and thus participates in the transcriptional regulation of Notch target genes, as well as regulation of the proliferation of PAGCs.

Epidermal G1-chalone and transforming growth factor-β are two different endogenous inhibitors of epidermal cell proliferation

1990 ◽  
Vol 142 (3) ◽  
pp. 496-504 ◽  
Author(s):  
K. Hartmut Richter ◽  
Ruben Schnapke ◽  
Matthias Clauss ◽  
Gerhard Fürstenberger ◽  
Detlef Hinz ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Epidermal Cell ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Endogenous Inhibitors ◽  
Epidermal Cell Proliferation

scholarly journals Evidence that gastropod torsion is driven by asymmetric cell proliferation activated by TGF-β signalling

2011 ◽  
Vol 7 (5) ◽  
pp. 759-762 ◽  
Author(s):  
Yoshihisa Kurita ◽  
Hiroshi Wada
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Driving Force ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Signalling Pathway ◽  
Retractor Muscle ◽  
Cast Doubt ◽  
The Right ◽  
Ontogenetic Process

Gastropods are characterized by their asymmetric bodyplan, which develops through a unique ontogenetic process called ‘torsion’. Despite several intensive studies, the driving force of torsion remains to be determined. Although torsion was traditionally believed to be driven by contraction of the retractor muscle connecting the foot and the shell, some recent reports cast doubt on that idea. Here, we report that torsion is accompanied by left–right asymmetric cell proliferation in the mantle epithelium in the limpet Nipponacmea fuscoviridis . Furthermore, we found that pharmacological inhibition of the transforming growth factor-β (TGF-β) signalling pathway, including that of Nodal, blocked torsion. We confirmed that the blocking was brought about through failure of the activation of cell proliferation in the right-hand side of the mantle epithelium, while the retractor muscle apparently developed normally. These results suggest that limpet torsion is driven by left–right asymmetric cell proliferation in the mantle epithelium, induced by the TGF-β pathway.

scholarly journals Latency-Associated Peptide of Transforming Growth Factor β Enhances Mycobacteriocidal Immunity in the Lung duringMycobacterium bovis BCG Infection in C57BL/6 Mice

2000 ◽  
Vol 68 (11) ◽  
pp. 6505-6508 ◽  
Author(s):  
K. A. Wilkinson ◽  
T. D. Martin ◽  
S. M. Reba ◽  
H. Aung ◽  
R. W. Redline ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Growth Factor ◽  
Mrna Expression ◽  
Mycobacterium Bovis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Gamma Interferon ◽  
T Cell Proliferation

ABSTRACT Latency-associated peptide of transforming growth factor β (TGF-β) (LAP) was used to determine whether in vivo modulation of TGF-β bioactivity enhanced pulmonary immunity to Mycobacterium bovis BCG infection in C57BL/6 mice. LAP decreased BCG growth in the lung and enhanced antigen-specific T-cell proliferation and gamma interferon mRNA expression. Thus, susceptibility of the lung to primary BCG infection may be partially mediated by the immunosuppressive effects of TGF-β.

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