Relationship between ETS Transcription Factor ETV1 and TGF-β-regulated SMAD Proteins in Prostate Cancer

Oh, Sangphil; Shin, Sook; Song, Hyohak; Grande, Joseph P.; Janknecht, Ralf

doi:10.1038/s41598-019-44685-3

Cited by 21 publications

(20 citation statements)

References 67 publications

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“…It is well accepted that TGF-β1 is mediated through both TGF-βR1 and TGF-βR2 receptors to induce phosphorylation of Smad2 and Smad3 [31][32][33][34]. Moreover, TGF-β1 can induce Smad7 expression, an inhibitory Smad family member, to negatively regulate TGF-β/Smad signaling pathway via a feedback regulation [35,36].…”

Section: Discussionmentioning

confidence: 99%

Effect of Jiawei Fengshining on Synovial Cell Apoptosis and TGF-β1/Smad Signaling Pathway in Rats with Rheumatoid Arthritis

Dong

Gao

Ding

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Background/Aims. Jiawei Fengshining (JWFSN) is a new formula originated from Fengshining, a classic formula for the treatment of rheumatoid arthritis (RA). The mechanism of JWFSN in the treatment of RA is still unclear. The aim of this study was to evaluate the effect of JWFSN formula on the inflammatory mediator levels in the serum and the TGF-β1/Smad pathway in the synovium and to explore the underlying mechanisms of JWFSN formula to ameliorate synovial hyperplasia and apoptosis inhibition of synovium in rats with RA. Method. SPF female Wistar rats were randomly divided into 6 groups: the blank control group, the model control group, the positive drug group, and the low-, medium-, and high- dose JWFSN groups, with 8 rats in each group. Enzyme-linked immunosorbent assay (ELISA) was used to detect inflammatory mediators, anti-inflammatory mediators, and rheumatoid factor (RF). The pathological condition and apoptosis of the synovial tissue were detected by hematoxylin and eosin (HE) and TUNEL staining, respectively. TGF-β1, p-Smad2, p-Smad3, and Smad7 protein expressions in synovial tissue were measured by western blot assay. In addition, human rheumatoid arthritis fibroblast-like synoviocytes cell line MH7A was treated with 20% JWFSN-containing serum to obtain in vitro data. Result. The administration of JWFSN was found to ameliorate synovial hyperplasia and promote apoptosis; increase the serum contents of anti-inflammatory mediators; reduce inflammatory mediators and RF contents; and inhibit the TGF-β1/Smad signaling pathway in CIA rats. In vitro JWFSN treatment increased the apoptosis of MH7A cells and decreased cell viability. Additionally, JWFSN treatment inhibited the TGF-β1/Smad signaling pathway in MH7A cells. Interestingly, kartogenin (TGF-β1/Smad pathway activator) treament reversed the effects of JWFSN treatment. Conclusion. JWFSN may ameliorate inflammatory factors’ abnormality, synovial hyperplasia, and apoptosis inhibition of synovium via the TGF-β1/Smad signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Effect of Jiawei Fengshining on Synovial Cell Apoptosis and TGF-β1/Smad Signaling Pathway in Rats with Rheumatoid Arthritis

Dong

Gao

Ding

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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“…Δhelk1 · enr was generated by in-frame C-terminal fusion of the Drosophila engrailed repressor region (EnR; Conlon et al ., 1996) to Δhelk1 , while enr · Δxetv1 was generated by in-frame N-terminal fusion of EnR to Δxetv1 . ΔΔxetv1 is deleted further in the N-terminal region of Δxetv1 to eliminate its DNA-binding capacity (Papoutsopoulou and Janknecht, 2000), thereby serving as a negative control construct. Structural features of the Ets proteins and their dominant-negative derivatives are shown in Fig.…”

Section: Methodsmentioning

confidence: 99%

Fgf/Ets signalling inXenopusectoderm initiates neural induction and patterning in an autonomous and paracrine manners

Hongo

Okamoto

2020

Preprint

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ABSTRACTFibroblast growth factor (Fgf) and anti-bone morphogenetic protein (Bmp) signals are derived from the organiser of mesoderm origin and cooperate to promote Xenopus neural development from the gastrula ectoderm. Using antisense oligos to Fgf2 and Fgf8 and dominant-negative Ets transcription factors, we showed that the expression of Fgf2, Fgf8, and Ets in ectoderm cells is essential to initiate neural induction both in vivo and in vitro. Our findings show that neural induction is initiated primarily by autonomous signalling in ectoderm cells, rather than by paracrine signalling from organiser cells. The signalling in ectoderm cells is transduced via the Fgf/Ras/Mapk/Ets pathway, independent of Bmp signal inhibition via the Fgf/Ras/Mapk/Smad1 route, as indicated by earlier studies. Through the same pathway, Fgfs activated position-specific neural genes dose-dependently along the anteroposterior axis in cultured ectoderm cells. The expression of these genes coincides with the establishment of the activated Ets gradient within the gastrula ectoderm. Organiser cells, being located posteriorly to the ectoderm, secrete Fgfs as gastrulation proceeds, which among several candidate molecules initially promote neural patterning of the induced neuroectoderm as morphogens.

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“…Differential expression analysis of two conditions was performed using version 3.16.5 of the edgeR software package 66 and the P values were adjusted using the Benjamini & Hochberg method. Validation of differentially expressed genes was done with RT-PCR 67 and visualization of amplified DNA fragments through ethidium-bromide staining 68 after agarose gel electrophoresis 69 . Respective primers are listed in Supplementary Information.…”

Section: In Vitro Protein Binding Assay Fusions Of Mdfi or Mdfic Witmentioning

confidence: 99%

Opposite Roles of the JMJD1A Interaction Partners MDFI and MDFIC in Colorectal Cancer

Yuan

et al. 2020

Sci Rep

Self Cite

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MyoD family inhibitor (MDfi) and MDfi domain-containing (MDfic) are homologous proteins known to regulate myogenic transcription factors. Hitherto, their role in cancer is unknown. We discovered that MDFI is up-and MDFIC downregulated in colorectal tumors. Mirroring these different expression patterns, MDFI stimulated and MDFIC inhibited growth of HCT116 colorectal cancer cells. Further, MDFI and MDFIC interacted with Jumonji C domain-containing (JMJD) 1 A, a histone demethylase and epigenetic regulator involved in colorectal cancer. JMJD1A influenced transcription of several genes that were also regulated by MDfi or MDfic. notably, the HIC1 tumor suppressor gene was stimulated by JMJD1A and MDFIC, but not by MDFI, and HIC1 overexpression phenocopied the growth suppressive effects of MDFIC in HCT116 cells. Similar to colorectal cancer, MDFI was up-and MDFIC downregulated in breast, ovarian and prostate cancer, but both were overexpressed in brain, gastric and pancreatic tumors that implies MDFIC to also promote tumorigenesis in certain tissues. Altogether, our data suggest a tumor modulating function for MDfi and MDfic in colorectal and other cancers that may involve their interaction with JMJD1A and a MDFIC→HIC1 axis.

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Relationship between ETS Transcription Factor ETV1 and TGF-β-regulated SMAD Proteins in Prostate Cancer

Cited by 21 publications

References 67 publications

Effect of Jiawei Fengshining on Synovial Cell Apoptosis and TGF-β1/Smad Signaling Pathway in Rats with Rheumatoid Arthritis

Effect of Jiawei Fengshining on Synovial Cell Apoptosis and TGF-β1/Smad Signaling Pathway in Rats with Rheumatoid Arthritis

Fgf/Ets signalling inXenopusectoderm initiates neural induction and patterning in an autonomous and paracrine manners

Opposite Roles of the JMJD1A Interaction Partners MDFI and MDFIC in Colorectal Cancer

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