Targeting the Vav3 oncogene enhances docetaxel-induced apoptosis through the inhibition of androgen receptor phosphorylation in LNCaP prostate cancer cells under chronic hypoxia

[1]  K. Matsuura,et al.  The Vav3 oncogene enhances the malignant potential of prostate cancer cells under chronic hypoxia. , 2014, Urologic oncology.

[2]  Mutsushi Yamasaki,et al.  Chronic hypoxia induces androgen-independent and invasive behavior in LNCaP human prostate cancer cells. , 2013, Urologic oncology.

[3]  K. Matsuura,et al.  Targeting the Vav3 oncogene enhances docetaxel-induced apoptosis through the inhibition of androgen receptor phosphorylation in LNCaP prostate cancer cells under chronic hypoxia , 2013, Molecular Cancer.

[4]  F. Hsu,et al.  The significance of Her2 on androgen receptor protein stability in the transition of androgen requirement in prostate cancer cells. , 2011, American journal of physiology. Endocrinology and metabolism.

[5]  Aristotelis Tsirigos,et al.  Understanding the "lethal" drivers of tumor-stroma co-evolution , 2010, Cancer biology & therapy.

[6]  Y. Kondo,et al.  Effect of the hsp90 inhibitor geldanamycin on androgen response of prostate cancer under hypoxic conditions , 2010, International journal of urology : official journal of the Japanese Urological Association.

[7]  C. Takimoto,et al.  Castration-Resistant Prostate Cancer: Locking Up the Molecular Escape Routes , 2009, Clinical Cancer Research.

[8]  Todd M Morgan,et al.  Targeted therapy for advanced prostate cancer: inhibition of the PI3K/Akt/mTOR pathway. , 2009, Current cancer drug targets.

[9]  N. Kyprianou,et al.  Androgen receptor and growth factor signaling cross-talk in prostate cancer cells. , 2008, Endocrine-related cancer.

[10]  S. McKeown,et al.  Hypoxia selects for androgen independent LNCaP cells with a more malignant geno‐ and phenotype , 2008, International journal of cancer.

[11]  G. Boivin,et al.  Targeted overexpression of vav3 oncogene in prostatic epithelium induces nonbacterial prostatitis and prostate cancer. , 2008, Cancer research.

[12]  F. Schröder,et al.  Progress in understanding androgen-independent prostate cancer (AIPC): a review of potential endocrine-mediated mechanisms. , 2008, European urology.

[13]  K. Burnstein,et al.  Ligand-independent activation of androgen receptors by Rho GTPase signaling in prostate cancer. , 2008, Molecular endocrinology.

[14]  M. Revelo,et al.  Vav3 oncogene is overexpressed and regulates cell growth and androgen receptor activity in human prostate cancer. , 2006, Molecular endocrinology.

[15]  W. Gerald,et al.  Combinatorial activities of Akt and B-Raf/Erk signaling in a mouse model of androgen-independent prostate cancer , 2006, Proceedings of the National Academy of Sciences.

[16]  K. Burnstein,et al.  Vav3, a Rho GTPase guanine nucleotide exchange factor, increases during progression to androgen independence in prostate cancer cells and potentiates androgen receptor transcriptional activity. , 2006, Molecular endocrinology.

[17]  Fuminori Tsuruta,et al.  JNK antagonizes Akt-mediated survival signals by phosphorylating 14-3-3 , 2005, The Journal of cell biology.

[18]  G. Hortobagyi,et al.  Docetaxel for treatment of solid tumours: a systematic review of clinical data. , 2005, The Lancet. Oncology.

[19]  C. Tangen,et al.  Docetaxel and estramustine compared with mitoxantrone and prednisone for advanced refractory prostate cancer. , 2004, The New England journal of medicine.

[20]  I. Tannock,et al.  Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer. , 2004, The New England journal of medicine.

[21]  S. Balk,et al.  Androgen receptor: A key molecule in the progression of prostate cancer to hormone independence , 2004, Journal of cellular biochemistry.

[22]  A. Alcover,et al.  Vav proteins, masters of the world of cytoskeleton organization. , 2004, Cellular signalling.

[23]  Esther B. E. Becker,et al.  Apoptosis Induced by p75NTR Overexpression Requires Jun Kinase-Dependent Phosphorylation of Bad , 2003, The Journal of Neuroscience.

[24]  K. Grigor,et al.  Androgen receptor gene amplification and protein expression in hormone refractory prostate cancer , 2003, British Journal of Cancer.

[25]  J. Simons,et al.  Androgens stimulate hypoxia-inducible factor 1 activation via autocrine loop of tyrosine kinase receptor/phosphatidylinositol 3'-kinase/protein kinase B in prostate cancer cells. , 2003, Clinical cancer research : an official journal of the American Association for Cancer Research.

[26]  X. Bustelo,et al.  Structural Determinants for the Biological Activity of Vav Proteins* , 2002, The Journal of Biological Chemistry.

[27]  L. Neckers,et al.  Hsp90 Regulates a von Hippel Lindau-independent Hypoxia-inducible Factor-1α-degradative Pathway* , 2002, The Journal of Biological Chemistry.

[28]  G. Raj,et al.  Guanosine phosphate binding protein coupled receptors in prostate cancer: a review. , 2002, The Journal of urology.

[29]  L. Neckers,et al.  Hsp90 regulates a von Hippel Lindau-independent hypoxia-inducible factor-1 alpha-degradative pathway. , 2002, The Journal of biological chemistry.

[30]  X. Bustelo.  Vav proteins, adaptors and cell signaling , 2001, Oncogene.

[31]  D. Feldman,et al.  The development of androgen-independent prostate cancer , 2001, Nature Reviews Cancer.

[32]  Fengqin Gao,et al.  Novel Role for JNK as a Stress-activated Bcl2 Kinase* , 2001, The Journal of Biological Chemistry.

[33]  J. Folkman,et al.  Vascular endothelial growth factor expression and tumor angiogenesis are regulated by androgens in hormone responsive human prostate carcinoma: evidence for androgen dependent destabilization of vascular endothelial growth factor transcripts. , 2001, The Journal of urology.

[34]  John D. Welsh,et al.  Vav3 Mediates Receptor Protein Tyrosine Kinase Signaling, Regulates GTPase Activity, Modulates Cell Morphology, and Induces Cell Transformation , 2000, Molecular and Cellular Biology.

[35]  X. Bustelo.  Regulatory and Signaling Properties of the Vav Family , 2000, Molecular and Cellular Biology.

[36]  Kazuhito Yamamoto,et al.  BCL-2 Is Phosphorylated and Inactivated by an ASK1/Jun N-Terminal Protein Kinase Pathway Normally Activated at G2/M , 1999, Molecular and Cellular Biology.

[37]  M. Scheid,et al.  Regulation of Bad Phosphorylation and Association with Bcl-xL by the MAPK/Erk Kinase* , 1999, The Journal of Biological Chemistry.

[38]  J. Isaacs,et al.  The biology of hormone refractory prostate cancer. Why does it develop? , 1999, The Urologic clinics of North America.

[39]  S. R. Datta,et al.  Akt Phosphorylation of BAD Couples Survival Signals to the Cell-Intrinsic Death Machinery , 1997, Cell.

[40]  J. Trapman,et al.  The androgen receptor in prostate cancer. , 1996, Pathology, research and practice.

[41]  T. Jacks,et al.  Cell proliferation, DNA repair, and p53 function are not required for programmed death of prostatic glandular cells induced by androgen ablation. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[42]  J. Folkman,et al.  Tumor angiogenesis and metastasis--correlation in invasive breast carcinoma. , 1991, The New England journal of medicine.

[43]  P. Scardino,et al.  Experimental oncogene induced prostate cancer. , 1991, Cancer surveys.

[44]  P. Goodman,et al.  A controlled trial of leuprolide with and without flutamide in prostatic carcinoma. , 1989, The New England journal of medicine.

[45]  M. Barbacid,et al.  vav, a novel human oncogene derived from a locus ubiquitously expressed in hematopoietic cells. , 1989, The EMBO journal.