Smad7 acts as a negative regulator of the epidermal growth factor (EGF) signaling pathway in breast cancer cells.
暂无分享,去创建一个
J. Lee | Sangmin Kim | Se Kyung Lee | S. Bae | S. Nam | Jee Soo Kim | Jung-Han Kim | J. Choe | Jung-Hyun Yang | M. Koo | D. Cho | Jeonghun Han | Min-young Choi | Min-Young Choi | Jun-Ho Choe
[1] K. Fujieda,et al. Transforming growth factor-beta1 induces matrix metalloproteinase-9 expression in human meningeal cells via ERK and Smad pathways. , 2009, Biochemical and biophysical research communications.
[2] Jeong Eon Lee,et al. EGF-induced MMP-9 expression is mediated by the JAK3/ERK pathway, but not by the JAK3/STAT-3 pathway in a SKBR3 breast cancer cell line. , 2009, Cellular signalling.
[3] M. Moasser,et al. The epidermal growth factor receptor family: Biology driving targeted therapeutics , 2008, Cellular and Molecular Life Sciences.
[4] K. Mohammad,et al. Stable overexpression of Smad7 in human melanoma cells impairs bone metastasis. , 2007, Cancer research.
[5] P. ten Dijke,et al. The tumor suppressor Smad4 is required for transforming growth factor beta-induced epithelial to mesenchymal transition and bone metastasis of breast cancer cells. , 2006, Cancer research.
[6] N. Normanno,et al. Epidermal growth factor receptor (EGFR) signaling in cancer. , 2006, Gene.
[7] K. Miyazono,et al. Effect of Smad7 expression on metastasis of mouse mammary carcinoma JygMC(A) cells. , 2005, Journal of the National Cancer Institute.
[8] L. Larue,et al. Stable overexpression of Smad7 in human melanoma cells inhibits their tumorigenicity in vitro and in vivo , 2005, Oncogene.
[9] Wei He,et al. Breast cancer bone metastasis mediated by the Smad tumor suppressor pathway. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[10] H. Dohlman,et al. MAPK kinase kinases (MKKKs) as a target class for small-molecule inhibition to modulate signaling networks and gene expression. , 2005, Current opinion in chemical biology.
[11] M. Björklund,et al. Gelatinase-mediated migration and invasion of cancer cells. , 2005, Biochimica et biophysica acta.
[12] S. Bao,et al. The activation of Akt/PKB signaling pathway and cell survival , 2005, Journal of cellular and molecular medicine.
[13] K. Choe,et al. Prognostic significance of the expression of Smad4 and Smad7 in human gastric carcinomas. , 2004, Annals of oncology : official journal of the European Society for Medical Oncology.
[14] Tony Hunter,et al. Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion. , 2003, Cancer cell.
[15] M. Sliwkowski,et al. An open-and-shut case? Recent insights into the activation of EGF/ErbB receptors. , 2003, Molecular cell.
[16] K. Flanders,et al. Smad3: A Key Player in Pathogenetic Mechanisms Dependent on TGF‐β , 2003, Annals of the New York Academy of Sciences.
[17] Koichi Hattori,et al. Angiogenesis: vascular remodeling of the extracellular matrix involves metalloproteinases , 2003, Current opinion in hematology.
[18] Z. Werb,et al. New functions for the matrix metalloproteinases in cancer progression , 2002, Nature Reviews Cancer.
[19] R. Herrmann,et al. Combined copy status of 18q21 genes in colorectal cancer shows frequent retention of SMAD7 , 2001, Genes, chromosomes & cancer.
[20] S. J. Chen,et al. Modulation of endogenous Smad expression in normal skin fibroblasts by transforming growth factor-beta. , 2000, Experimental cell research.
[21] M. Bitzer,et al. Smad3 and Smad4 Mediate Transcriptional Activation of the Human Smad7 Promoter by Transforming Growth Factor β* , 2000, The Journal of Biological Chemistry.
[22] H. Modjtahedi,et al. Epidermal growth factor-like ligands differentially up-regulate matrix metalloproteinase 9 in head and neck squamous carcinoma cells. , 2000, Cancer research.
[23] L. Coussens,et al. Extrinsic regulators of epithelial tumor progression: metalloproteinases. , 2000, Current opinion in genetics & development.
[24] D. Crowe,et al. Transcriptional inhibition of matrix metalloproteinase 9 (MMP-9) activity by a c-fos/estrogen receptor fusion protein is mediated by the proximal AP-1 site of the MMP-9 promoter and correlates with reduced tumor cell invasion. , 1999, Neoplasia.
[25] H. Friess,et al. The TGF-β signaling inhibitor Smad7 enhances tumorigenicity in pancreatic cancer , 1999, Oncogene.
[26] J. Massagué,et al. Inhibition of transforming growth factor-β/SMAD signalling by the interferon-γ/STAT pathway , 1999, Nature.
[27] M. Stack,et al. Proteinase requirements of epidermal growth factor–induced ovarian cancer cell invasion , 1998, International journal of cancer.
[28] C. Heldin,et al. Induction of inhibitory Smad6 and Smad7 mRNA by TGF-beta family members. , 1998, Biochemical and biophysical research communications.
[29] A. Roberts,et al. Smad2 transduces common signals from receptor serine-threonine and tyrosine kinases. , 1998, Genes & development.
[30] T. Pawson,et al. Signaling through scaffold, anchoring, and adaptor proteins. , 1997, Science.
[31] R. Fridman,et al. Epidermal growth factor and amphiregulin up‐regulate matrix metalloproteinase‐9 (MMP‐9) in human breast cancer cells , 1997, International journal of cancer.
[32] G. Stark,et al. Regulation of STAT‐dependent pathways by growth factors and cytokines , 1996, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[33] N. Normanno,et al. Epidermal growth factor-related peptides and their receptors in human malignancies. , 1995, Critical reviews in oncology/hematology.
[34] J. Massagué,et al. Disruption of transforming growth factor beta signaling by a mutation that prevents transphosphorylation within the receptor complex , 1995, Molecular and cellular biology.
[35] T. Tsuruo,et al. Serum and plasma M(r) 92,000 progelatinase levels correlate with spontaneous metastasis of rat 13762NF mammary adenocarcinoma. , 1993, Cancer research.
[36] D. Crowe,et al. Jun N-terminal kinase 1 mediates transcriptional induction of matrix metalloproteinase 9 expression. , 2001, Neoplasia.
[37] Y. Yarden,et al. Biochemical and clinical implications of the ErbB/HER signaling network of growth factor receptors. , 2000, Advances in cancer research.