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: Development. 2006 Feb 15; [Epub ahead of print]

Related Articles, Links


(2006)NF-{kappa}B transmits Eda A1/EdaR signalling to activate Shh and cyclin D1 expression, and controls post-initiation hair placode down growth.

Schmidt-Ullrich R, Tobin DJ, Lenhard D, Schneider P, Paus R, Scheidereit C.

A novel function of NF-kappaB in the development of most ectodermal appendages, including two types of murine pelage hair follicles, was detected in a mouse model with suppressed NF-kappaB activity (c(IkappaBalphaDeltaN)). However, the developmental processes regulated by NF-kappaB in hair follicles has remained unknown. Furthermore, the similarity between the phenotypes of c(IkappaBADeltaN) mice and mice deficient in Eda A1 (tabby) or its receptor EdaR (downless) raised the issue of whether in vivo NF-kappaB regulates or is regulated by these novel TNF family members. We now demonstrate that epidermal NF-kappaB activity is first observed in placodes of primary guard hair follicles at day E14.5, and that in vivo NF-kappaB signalling is activated downstream of Eda A1 and EdaR. Importantly, ectopic signals which activate NF-kappaB can also stimulate guard hair placode formation, suggesting a crucial role for NF-kappaB in placode development. In downless and c(IkappaBalphaDeltaN) mice, placodes start to develop, but rapidly abort in the absence of EdaR/NF-kappaB signalling. We show that NF-kappaB activation is essential for induction of Shh and cyclin D1 expression and subsequent placode down growth. However, cyclin D1 induction appears to be indirectly regulated by NF-kappaB, probably via Shh and Wnt. The strongly decreased number of hair follicles observed in c(IkappaBalphaDeltaN) mice compared with tabby mice, indicates that additional signals, such as TROY, must regulate NF-kappaB activity in specific hair follicle subtypes.

PMID: 16481354 [PubMed - as supplied by publisher]

 

 

 

 

 

AIM: To examine the expression of Egr-1, c-fos and cyclin D1 at both transcript and protein levels in esophageal carcinoma and to correlate the level of their expressions with precancerous and paracancerous esophageal lesions and esophageal carcinoma. METHODS: In situ hybridization and immunohistochemistry were used respectively to detect the expression of mRNA and proteins of Egr-1, c-fos and cyclin D1 in 70 cases of esophageal squamous cell carcinoma and their corresponding para-cancerous mucosa and upper cut edge mucosa. RESULTS: In situ hybridization and immunohistochemistry showed positive staining of all three mRNAs in the cytoplasm and those of the proteins in nuclei. Overexpression of Egr-1, c-fos and cyclin D1 mRNAs and their proteins was found in dysplasia and squamous carcinomas. The expression level of Egr-1 and c-fos was high, and cyclin D1 was low in dysplasia mucosa, whereas the expression of Egr-1 was decreased, c-fos was maintained and cyclin D1 was increased in the cancers. The expression of both c-fos and cyclinD1 was consistent between the mRNA and protein in their corresponding high expression lesions. CONCLUSION: The expression of Egr-1, c-fos and cyclin D1 varies in esophageal precancerous lesions and cancer tissues, suggesting an involvement of these genes in the development of esophageal carcinoma.

PMID: 14966901 [PubMed - in process]