IL-6 promotes prostate tumorigenesis and progression through autocrine cross-activation of IGF-IR

[1]  J. Pinski,et al.  Clinical and Correlative Results of SWOG S0354: A Phase II Trial of CNTO328 (Siltuximab), a Monoclonal Antibody against Interleukin-6, in Chemotherapy-Pretreated Patients with Castration-Resistant Prostate Cancer , 2010, Clinical Cancer Research.

[2]  Y. DeClerck,et al.  Interleukin-6 in bone metastasis and cancer progression. , 2010, European journal of cancer.

[3]  Z. Culig,et al.  Interleukin-6 trans-signalling differentially regulates proliferation, migration, adhesion and maspin expression in human prostate cancer cells , 2010, Endocrine-related cancer.

[4]  T. Mak,et al.  Disruption of the Lcn2 gene in mice suppresses primary mammary tumor formation but does not decrease lung metastasis , 2010, Proceedings of the National Academy of Sciences.

[5]  R. Huang,et al.  Epithelial-Mesenchymal Transitions in Development and Disease , 2009, Cell.

[6]  E. Petricoin,et al.  Periprostatic adipose tissue as a modulator of prostate cancer aggressiveness. , 2009, The Journal of urology.

[7]  Y. Nagashima,et al.  aPKCλ/ι promotes growth of prostate cancer cells in an autocrine manner through transcriptional activation of interleukin-6 , 2009, Proceedings of the National Academy of Sciences.

[8]  F. Vesuna,et al.  Interleukin-6 induces an epithelial–mesenchymal transition phenotype in human breast cancer cells , 2009, Oncogene.

[9]  E. Platz,et al.  Anti-inflammatory drugs, antioxidants, and prostate cancer prevention. , 2009, Current opinion in pharmacology.

[10]  E. Neilson,et al.  Biomarkers for epithelial-mesenchymal transitions. , 2009, The Journal of clinical investigation.

[11]  H. Werner,et al.  The insulin-like growth factor-I receptor as an oncogene , 2009, Archives of physiology and biochemistry.

[12]  D. Zurakowski,et al.  Lipocalin 2 promotes breast cancer progression , 2009, Proceedings of the National Academy of Sciences.

[13]  Z. Zehner,et al.  Inhibition of vimentin or β1 integrin reverts morphology of prostate tumor cells grown in laminin-rich extracellular matrix gels and reduces tumor growth in vivo , 2009, Molecular Cancer Therapeutics.

[14]  M. Karin,et al.  IL-6 and Stat3 are required for survival of intestinal epithelial cells and development of colitis-associated cancer. , 2009, Cancer cell.

[15]  Y. Furuya,et al.  Implications of insulin‐like growth factor‐I for prostate cancer therapies , 2009, International journal of urology : official journal of the Japanese Urological Association.

[16]  C. Riley,et al.  Cross talk of signals between EGFR and IL-6R through JAK2/STAT3 mediate epithelial–mesenchymal transition in ovarian carcinomas , 2008, British Journal of Cancer.

[17]  Robert A. Weinberg,et al.  Ras oncogenes: split personalities , 2008, Nature Reviews Molecular Cell Biology.

[18]  T. Ratliff,et al.  Prostate inflammation and its potential impact on prostate cancer: A current review , 2008, Journal of cellular biochemistry.

[19]  J. Bartlett,et al.  An Increase in N-Ras Expression is Associated with Development of Hormone Refractory Prostate Cancer in a Subset of Patients , 2008, Disease markers.

[20]  M. Karin,et al.  Autocrine IL-6 signaling: a key event in tumorigenesis? , 2008, Cancer cell.

[21]  C. Stewart,et al.  Beneficial synergistic interactions of TNF-α and IL-6 in C2 skeletal myoblasts—Potential cross-talk with IGF system , 2008, Growth factors.

[22]  D. Belpomme,et al.  Overweight/obesity and cancer genesis: more than a biological link. , 2007, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.

[23]  D. Ludwig,et al.  IMC-A12, a Human IgG1 Monoclonal Antibody to the Insulin-Like Growth Factor I Receptor , 2007, Clinical Cancer Research.

[24]  R. Beyer,et al.  Comparison of the cytotoxicity of the nitroaromatic drug flutamide to its cyano analogue in the hepatocyte cell line TAMH: evidence for complex I inhibition and mitochondrial dysfunction using toxicogenomic screening. , 2007, Chemical research in toxicology.

[25]  J. Bartlett,et al.  Expression levels of the JAK/STAT pathway in the transition from hormone-sensitive to hormone-refractory prostate cancer , 2007, British Journal of Cancer.

[26]  S. Terry,et al.  The NF-κB/IL-6 pathway in metastatic androgen-independent prostate cancer: new therapeutic approaches? , 2007, World Journal of Urology.

[27]  E. Platz,et al.  Inflammation in the etiology of prostate cancer: an epidemiologic perspective. , 2007, Urologic oncology.

[28]  Jianfeng Xu,et al.  Inflammation in prostate carcinogenesis , 2007, Nature Reviews Cancer.

[29]  S. Taneja,et al.  Obesity and prostate cancer. , 2006, The Canadian journal of urology.

[30]  G. Duigou,et al.  Targeting gene expression selectively in cancer cells by using the progression-elevated gene-3 promoter. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[31]  Stefan Wirtz,et al.  TGF-β Suppresses Tumor Progression in Colon Cancer by Inhibition of IL-6 trans-Signaling , 2004 .

[32]  R. Kiesslich,et al.  TGF-beta suppresses tumor progression in colon cancer by inhibition of IL-6 trans-signaling. , 2004, Immunity.

[33]  J. Massagué,et al.  Epithelial-Mesenchymal Transitions Twist in Development and Metastasis , 2004, Cell.

[34]  Peter Bohlen,et al.  A fully human monoclonal antibody to the insulin-like growth factor I receptor blocks ligand-dependent signaling and inhibits human tumor growth in vivo. , 2003, Cancer research.

[35]  A. Costello,et al.  Interleukin‐6: minor player or starring role in the development of hormone‐refractory prostate cancer? , 2003, BJU international.

[36]  J. Thiery Epithelial–mesenchymal transitions in tumour progression , 2002, Nature Reviews Cancer.

[37]  R. Tibshirani,et al.  Significance analysis of microarrays applied to the ionizing radiation response , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[38]  Z. Su,et al.  PEA3 sites within the progression elevated gene-3 (PEG-3) promoter and mitogen-activated protein kinase contribute to differential PEG-3 expression in Ha-ras and v-raf oncogene transformed rat embryo cells. , 2001, Nucleic acids research.

[39]  P. Fisher,et al.  Cooperation between AP1 and PEA3 sites within the progression elevated gene-3 (PEG-3) promoter regulate basal and differential expression of PEG-3 during progression of the oncogenic phenotype in transformed rat embryo cells , 2000, Oncogene.

[40]  Y. Horiguchi,et al.  Serum interleukin 6 as a prognostic factor in patients with prostate cancer. , 2000, Clinical cancer research : an official journal of the American Association for Cancer Research.

[41]  L. Flechner,et al.  Insulin-Like Growth Factor I Synergizes with Interleukin 4 for Hematopoietic Cell Proliferation Independent of Insulin Receptor Substrate Expression , 1999, Molecular and Cellular Biology.

[42]  Z. Su,et al.  Subtraction hybridization identifies a transformation progression-associated gene PEG-3 with sequence homology to a growth arrest and DNA damage-inducible gene. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[43]  C. Jackson-Cook,et al.  Tumorigenicity of SV40 T antigen immortalized human prostate epithelial cells: Association with decreased epidermal growth factor receptor (EGFR) expression , 1994, International journal of cancer.

[44]  E. Platz,et al.  Obesity and prostate cancer: making sense out of apparently conflicting data. , 2007, Epidemiologic reviews.

[45]  S. Terry,et al.  The NF-kappaB/IL-6 pathway in metastatic androgen-independent prostate cancer: new therapeutic approaches? , 2007, World journal of urology.

[46]  R. Bast,et al.  Use of Ras-transformed human ovarian surface epithelial cells as a model for studying ovarian cancer. , 2006, Methods in enzymology.

[47]  C. Morrissey,et al.  Prostate epithelial cell differentiation and its relevance to the understanding of prostate cancer therapies. , 2005, Clinical science.

[48]  S. Plymate,et al.  Transcriptional regulation of insulin-like growth factor-I receptor gene expression in prostate cancer cells. , 2001, Endocrinology.