A positive role for Myc in TGFβ-induced Snail transcription and epithelial-to-mesenchymal transition

Smith, Andrew P.; Verrecchia, Alessandro; Fagà, Giovanni; Doni, Mirko; Perna, Daniele; Martinato, Francesca; Guccione, Ernesto; Amati, Bruno

doi:10.1038/onc.2008.395

Cited by 117 publications

(92 citation statements)

References 53 publications

(68 reference statements)

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“…Consistent with a recent report (Smith et al, 2009), we observed TGF-dependent induction of SNAIL in MDA-MB231 cells. Similarly, we detected that TGF activates expression of SLUG, PAI-1 and SMAD7 in an IKK-dependent fashion.…”

Section: Fig 4 Tgf-dependent Downregulation Of E-cadherin Is Nfb-supporting

confidence: 82%

IKKα controls canonical TGFβ–SMAD signaling to regulate genes expressing SNAIL and SLUG during EMT in Panc1 cells

Brandl

Seidler

Haller

et al. 2010

Journal of Cell Science

115

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There was an error published in J. Cell Sci. 123, 4231-4239.In Fig. 4A, the cRel siRNA western blot panel was inadvertently constructed using the wrong images and all three western blots showed incorrect loading controls. The correct images and loading controls are shown in the figure below. The mistake in the figure did not affect the conclusions of the paper.We apologise for this mistake. . TGFb-dependent downregulation of E-cadherin is NFkB-independent. (A) Panc1 cells were transfected with a control or RelA/p65-, RelB-or c-Relspecific siRNA. At 24 hours after the transfection, cells were treated with 10 ng/ml TGFb or were left as an untreated control in DMEM without FCS. After an additional 48 hours, western blots detected RelA/p65, RelB or c-Rel and E-cadherin expression. The membrane was stripped and probed for a-tubulin or b-actin to ensure equal protein loading. (B) Panc1 (upper graph) and MDA-MB231 cells (lower graph) cells were co-transfected with a control or IKKa-specific siRNA and 500 ng of the pGL3control-, NFkB-or SMAD-luciferase reporter gene constructs as indicated. At 24 hours after the transfection, cells were treated with 10 ng/ml TGFb or were left as an untreated control. Luciferase activity was measured 6 hours after the TGFb treatment (Student's t-test: *P,0.05 versus control). (C) Panc1 (upper graph) and MDA-MB231 (lower graph) cells were transfected with a control or IKKa-specific siRNA. At 48 hours after the transfection, cells were stimulated with TGFb (10 ng/ml) for 20 minutes and binding of SMAD3 and SMAD4 to a SMAD consensus oligonucleotide was detected using ABCD assays. Input represents 5% of whole-cell extract of control siRNA-transfected cells. (D) Panc1 cells were treated as in C. Immunoprecipitation was performed with an IKKa-specific antibody or pre-immune serum as a control. Western blots of immunoprecipitates were probed with antibodies against IKKa and SMAD3. Input represents 5% of whole-cell extract of control siRNA-transfected Panc1 cells. (E) MDA-MB231 cells were transfected with a control or IKKa-specific siRNA. At 24 hours after the transfection, cells were treated with 10 ng/ml TGFb or were left as an untreated control in DMEM without FCS. After an additional 48 hours, western blots detected IKKa expression. The membrane was stripped and probed for b-actin to ensure equal protein loading.

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Section: Fig 4 Tgf-dependent Downregulation Of E-cadherin Is Nfb-supporting

confidence: 82%

IKKα controls canonical TGFβ–SMAD signaling to regulate genes expressing SNAIL and SLUG during EMT in Panc1 cells

Brandl

Seidler

Haller

et al. 2010

Journal of Cell Science

115

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“…Using quantitative ChIP analysis, Smad2 and Smad3 were found to directly target the Snail promoter, but no significant enrichment of Smad4 was detected (45). It has also been reported that, during keratinocyte proliferation and differentiation, the nuclear accumulation of activated Smad2/3 is Smad4-independent, and IB kinase ␣ (IKK␣) but not Smad4 serves as a nuclear cofactor for Smad2/3 recruitment to Mad1 chromatin in epidermis (46).…”

Section: Discussionmentioning

confidence: 99%

An Atypical Canonical Bone Morphogenetic Protein (BMP) Signaling Pathway Regulates Msh Homeobox 1 (Msx1) Expression during Odontogenesis

Yang

Yuan

et al. 2014

Journal of Biological Chemistry

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Background: BMP signaling regulates expression of the odontogenic gene Msx1 in dental mesenchyme. Results: Canonical BMP signaling is not operating in early developing tooth, and Smad1/5 but not Smad4 are required for BMP-induced Msx1 expression in dental mesenchymal cells. Conclusion: BMP/Smads regulation of Msx1 expression is Smad4-independent. Significance: A novel atypical canonical BMP signaling is identified to regulate tooth development.

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“…The Myc proteins are involved in major biological processes including proliferation, metabolism, cell cycle progression, apoptosis, cell growth and differentiation, fibrosis, and polarity (34)(35)(36) (Figure 1). All of these cellular functions are altered and ongoing in ADPKD.…”

Section: Myc Cellular Functionsmentioning

confidence: 99%

c-Myc Signalling in the Genetic Mechanism of Polycystic Kidney Disease

Trudel

2015

Polycystic Kidney Disease

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Licence: This open access article is licenced under Creative Commons Attribution 4.0 International (CC BY 4.0). http://creativecommons.org/licenses/by/4.0/ Users are allowed to share (copy and redistribute the material in any medium or format) and adapt (remix, transform, and build upon the material for any purpose, even commercially), as long as the author and the publisher are explicitly identified and properly acknowledged as the original source. AbstractThe Myc family of transcription factors regulates major biological processes such as proliferation, stem/progenitor cell pluripotency, metabolism, apoptosis, cell growth and differentiation. The most-studied member c-Myc is essential in embryonic development and cellular homeostasis. Dysregulation of c-Myc protein function is not only associated with malignant transformation and human tumors but is also implicated in autosomal dominant polycystic kidney disease (ADPKD), a human genetic disorder, considered a neoplasia in disguise. Studies from human ADPKD kidneys, caused by mutation in the

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A positive role for Myc in TGFβ-induced Snail transcription and epithelial-to-mesenchymal transition

Cited by 117 publications

References 53 publications

IKKα controls canonical TGFβ–SMAD signaling to regulate genes expressing SNAIL and SLUG during EMT in Panc1 cells

IKKα controls canonical TGFβ–SMAD signaling to regulate genes expressing SNAIL and SLUG during EMT in Panc1 cells

An Atypical Canonical Bone Morphogenetic Protein (BMP) Signaling Pathway Regulates Msh Homeobox 1 (Msx1) Expression during Odontogenesis

c-Myc Signalling in the Genetic Mechanism of Polycystic Kidney Disease

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