The tumor suppressor Smad4 is required for transforming growth factor beta-induced epithelial to mesenchymal transition and bone metastasis of breast cancer cells.
about
Hypoxia and TGF-beta drive breast cancer bone metastases through parallel signaling pathways in tumor cells and the bone microenvironment.Hyaluronan synthase 2 (HAS2) promotes breast cancer cell invasion by suppression of tissue metalloproteinase inhibitor 1 (TIMP-1)Antagonistic regulation of EMT by TIF1γ and Smad4 in mammary epithelial cellsIn situ proximity ligation detection of c-Jun/AP-1 dimers reveals increased levels of c-Jun/Fra1 complexes in aggressive breast cancer cell lines in vitro and in vivoHomeodomain protein DLX4 counteracts key transcriptional control mechanisms of the TGF-β cytostatic program and blocks the antiproliferative effect of TGF-βMicroRNA-155 is regulated by the transforming growth factor beta/Smad pathway and contributes to epithelial cell plasticity by targeting RhoAThe Roles of Epithelial-to-Mesenchymal Transition (EMT) and Mesenchymal-to-Epithelial Transition (MET) in Breast Cancer Bone Metastasis: Potential Targets for Prevention and TreatmentRegulation of epithelial-mesenchymal transition through SUMOylation of transcription factorsMolecular mechanisms of epithelial-mesenchymal transitionDPC4 gene status of the primary carcinoma correlates with patterns of failure in patients with pancreatic cancer.Implications of Hypoxia in Breast Cancer Metastasis to BoneRole of TGFβ in regulation of the tumor microenvironment and drug delivery (review)Transforming Growth Factor-Beta and Oxidative Stress Interplay: Implications in Tumorigenesis and Cancer ProgressionSmad2 and Smad3 have opposing roles in breast cancer bone metastasis by differentially affecting tumor angiogenesisSmad4-dependent desmoglein-4 expression contributes to hair follicle integrityTGF-beta-induced epithelial to mesenchymal transitionInvolvement of Ras GTPase-activating protein SH3 domain-binding protein 1 in the epithelial-to-mesenchymal transition-induced metastasis of breast cancer cells via the Smad signaling pathway.Loss of BRMS1 promotes a mesenchymal phenotype through NF-κB-dependent regulation of Twist1.A complex containing LPP and α-actinin mediates TGFβ-induced migration and invasion of ErbB2-expressing breast cancer cells.BMP7: a new bone metastases prevention?Atlas of Cancer Signalling Network: a systems biology resource for integrative analysis of cancer data with Google MapsBMP-6 promotes E-cadherin expression through repressing deltaEF1 in breast cancer cells.The properties of high-dimensional data spaces: implications for exploring gene and protein expression data.The DPC4/SMAD4 genetic status determines recurrence patterns and treatment outcomes in resected pancreatic ductal adenocarcinoma: A prospective cohort study.Suppression of TGFβ-induced epithelial-mesenchymal transition like phenotype by a PIAS1 regulated sumoylation pathway in NMuMG epithelial cells.Annexin A1 regulates TGF-beta signaling and promotes metastasis formation of basal-like breast cancer cells.The regulation of TGF-β/SMAD signaling by protein deubiquitination.Targeting the Transforming Growth Factor-beta pathway inhibits human basal-like breast cancer metastasis.SMAD4 is a potential prognostic marker in human breast carcinomas.TGF-β1 signaling targets metastasis-associated protein 1, a new effector in epithelial cellsTumor-supportive and osteoclastogenic changes induced by breast cancer-derived factors are reversed by inhibition of {gamma}-secretase.Progesterone receptor activates Msx2 expression by downregulating TNAP/Akp2 and activating the Bmp pathway in EpH4 mouse mammary epithelial cells.Tgf-beta signaling pathway in lung adenocarcinoma invasion.PARP-1 regulates epithelial-mesenchymal transition (EMT) in prostate tumorigenesisHDAC6 deacetylase activity is required for hypoxia-induced invadopodia formation and cell invasion.Klf4 is a transcriptional regulator of genes critical for EMT, including Jnk1 (Mapk8).Role of SIRT1 in regulation of epithelial-to-mesenchymal transition in oral squamous cell carcinoma metastasisPancreatic cancer cells respond to type I collagen by inducing snail expression to promote membrane type 1 matrix metalloproteinase-dependent collagen invasion.Roles for growth factors in cancer progression.Transforming growth factor-β and the hallmarks of cancer.
P2860
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P2860
The tumor suppressor Smad4 is required for transforming growth factor beta-induced epithelial to mesenchymal transition and bone metastasis of breast cancer cells.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
@zh
2006年论文
@zh-cn
name
The tumor suppressor Smad4 is ...... stasis of breast cancer cells.
@en
type
label
The tumor suppressor Smad4 is ...... stasis of breast cancer cells.
@en
prefLabel
The tumor suppressor Smad4 is ...... stasis of breast cancer cells.
@en
P2093
P50
P1433
P1476
The tumor suppressor Smad4 is ...... stasis of breast cancer cells.
@en
P2093
Jeroen Buijs
Maarten van Dinther
Martine Deckers
Peter ten Dijke
P304
P356
10.1158/0008-5472.CAN-05-3560
P407
P577
2006-02-01T00:00:00Z