ASC-J9® suppresses prostate cancer cell proliferation and invasion via altering the ATF3-PTK2 signaling

[1]  S. Yeh,et al.  Preclinical study using androgen receptor (AR) degradation enhancer to increase radiotherapy efficacy via targeting radiation-increased AR to better suppress prostate cancer progression , 2019, EBioMedicine.

[2]  A. Jemal,et al.  Cancer statistics, 2019 , 2019, CA: a cancer journal for clinicians.

[3]  S. Amin,et al.  Phenylbutyl isoselenocyanate induces reactive oxygen species to inhibit androgen receptor and to initiate p53‐mediated apoptosis in LNCaP prostate cancer cells , 2018, Molecular carcinogenesis.

[4]  Chawnshang Chang,et al.  ASC-J9® suppresses prostate cancer cell invasion via altering the sumoylation-phosphorylation of STAT3. , 2018, Cancer letters.

[5]  S. Gou,et al.  Theranostic Pt(IV) Conjugate with Target Selectivity for Androgen Receptor. , 2018, Inorganic chemistry.

[6]  S. Yeh,et al.  Androgen receptor (AR) degradation enhancer ASC-J9® in an FDA-approved formulated solution suppresses castration resistant prostate cancer cell growth. , 2018, Cancer letters.

[7]  W. El-Deiry,et al.  ONC201 Targets AR and AR-V7 Signaling, Reduces PSA, and Synergizes with Everolimus in Prostate Cancer , 2018, Molecular Cancer Research.

[8]  G. Park,et al.  Cytotoxic activity of the twigs of Cinnamomum cassia through the suppression of cell proliferation and the induction of apoptosis in human colorectal cancer cells , 2018, BMC Complementary and Alternative Medicine.

[9]  S. Tsui,et al.  RNA-Seq revealed ATF3-regulated inflammation induced by silica. , 2018, Toxicology.

[10]  David J. Arenillas,et al.  JASPAR 2018: update of the open-access database of transcription factor binding profiles and its web framework , 2017, Nucleic acids research.

[11]  David J. Arenillas,et al.  JASPAR 2018: update of the open-access database of transcription factor binding profiles and its web framework , 2017, Nucleic Acids Res..

[12]  S. Yeh,et al.  Androgen-deprivation therapy with enzalutamide enhances prostate cancer metastasis via decreasing the EPHB6 suppressor expression. , 2017, Cancer letters.

[13]  Jun Luo,et al.  Preclinical Study using Malat1 Small Interfering RNA or Androgen Receptor Splicing Variant 7 Degradation Enhancer ASC-J9® to Suppress Enzalutamide-resistant Prostate Cancer Progression. , 2017, European urology.

[14]  Jiaoti Huang,et al.  Loss of SPDEF and gain of TGFBI activity after androgen deprivation therapy promote EMT and bone metastasis of prostate cancer , 2017, Science Signaling.

[15]  N. Terada,et al.  Effect of propofol on androgen receptor activity in prostate cancer cells , 2017, European journal of pharmacology.

[16]  Wei Yu Chen,et al.  Inhibition of the androgen receptor induces a novel tumor promoter, ZBTB46, for prostate cancer metastasis , 2017, Oncogene.

[17]  Dakang Xu,et al.  Overexpression of the transcription factor ATF3 with a regulatory molecular signature associates with the pathogenic development of colorectal cancer , 2017, Oncotarget.

[18]  Chawnshang Chang,et al.  Sorafenib with ASC‐J9® synergistically suppresses the HCC progression via altering the pSTAT3‐CCL2/Bcl2 signals , 2016, International journal of cancer.

[19]  M. Lappas,et al.  ATF3 is a negative regulator of inflammation in human fetal membranes. , 2016, Placenta.

[20]  Chawnshang Chang,et al.  ASC-J9(®) suppresses castration resistant prostate cancer progression via degrading the enzalutamide-induced androgen receptor mutant AR-F876L. , 2016, Cancer letters.

[21]  Sherry L. Werner,et al.  Dual targeting of androgen receptor and mTORC1 by salinomycin in prostate cancer , 2016, Oncotarget.

[22]  Dingfang Cai,et al.  Echinacoside Protects Against MPP+-Induced Neuronal Apoptosis via ROS/ATF3/CHOP Pathway Regulation , 2016, Neuroscience Bulletin.

[23]  Y. Kanai,et al.  Up-Regulation of LAT1 during Antiandrogen Therapy Contributes to Progression in Prostate Cancer Cells. , 2016, The Journal of urology.

[24]  Seong-ho Lee,et al.  Potential Dual Role of Activating Transcription Factor 3 in Colorectal Cancer. , 2016, Anticancer research.

[25]  S. Yeh,et al.  TNF signaling mediates an enzalutamide-induced metastatic phenotype of prostate cancer and microenvironment cell co-cultures , 2015, Oncotarget.

[26]  Hong-Chiang Chang,et al.  Stromal androgen receptor roles in the development of normal prostate, benign prostate hyperplasia, and prostate cancer. , 2015, The American journal of pathology.

[27]  C. Creighton,et al.  Androgen deprivation-induced NCoA2 promotes metastatic and castration-resistant prostate cancer. , 2014, The Journal of clinical investigation.

[28]  E. Li,et al.  ATF3 functions as a novel tumor suppressor with prognostic significance in esophageal squamous cell carcinoma , 2014, Oncotarget.

[29]  D. Schlaepfer,et al.  FAK in cancer: mechanistic findings and clinical applications , 2014, Nature Reviews Cancer.

[30]  F. Gramatica,et al.  Antiproliferative effect of ASC-J9 delivered by PLGA nanoparticles against estrogen-dependent breast cancer cells. , 2014, Molecular pharmaceutics.

[31]  Y. Maehara,et al.  Role of Activating Transcription Factor 3 (ATF3) in Endoplasmic Reticulum (ER) Stress-induced Sensitization of p53-deficient Human Colon Cancer Cells to Tumor Necrosis Factor (TNF)-related Apoptosis-inducing Ligand (TRAIL)-mediated Apoptosis through Up-regulation of Death Receptor 5 (DR5) by Zerumbo , 2014, The Journal of Biological Chemistry.

[32]  S. Yeh,et al.  Determination of androgen receptor degradation enhancer ASC-J9(®) in mouse sera and organs with liquid chromatography tandem mass spectrometry. , 2014, Journal of pharmaceutical and biomedical analysis.

[33]  Chawnshang Chang,et al.  Targeting inflammatory cytokines-androgen receptor (AR) signaling with ASC-J9® to better battle prostate cancer progression , 2013, Oncoimmunology.

[34]  Yiling Bi,et al.  Induction of DNA damage and ATF3 by retigeric acid B, a novel topoisomerase II inhibitor, promotes apoptosis in prostate cancer cells. , 2013, Cancer letters.

[35]  S. Yeh,et al.  Anti-androgen receptor ASC-J9 versus anti-androgens MDV3100 (Enzalutamide) or Casodex (Bicalutamide) leads to opposite effects on prostate cancer metastasis via differential modulation of macrophage infiltration and STAT3-CCL2 signaling , 2013, Cell Death and Disease.

[36]  Dakang Xu,et al.  ATF3 suppresses metastasis of bladder cancer by regulating gelsolin-mediated remodeling of the actin cytoskeleton. , 2013, Cancer research.

[37]  Chawnshang Chang,et al.  Androgen receptor roles in the development of benign prostate hyperplasia. , 2013, The American journal of pathology.

[38]  S. Yeh,et al.  Differential Androgen Deprivation Therapies with Anti-androgens Casodex/Bicalutamide or MDV3100/Enzalutamide versus Anti-androgen Receptor ASC-J9® Lead to Promotion versus Suppression of Prostate Cancer Metastasis* , 2013, The Journal of Biological Chemistry.

[39]  J. Hung,et al.  Subamolide A Induces Mitotic Catastrophe Accompanied by Apoptosis in Human Lung Cancer Cells , 2013, Evidence-based complementary and alternative medicine : eCAM.

[40]  S. Yeh,et al.  New therapeutic approach to suppress castration-resistant prostate cancer using ASC-J9 via targeting androgen receptor in selective prostate cells. , 2013, The American journal of pathology.

[41]  Kyle J. Kiriluk,et al.  Sox2 Is an Androgen Receptor-Repressed Gene That Promotes Castration-Resistant Prostate Cancer , 2013, PloS one.

[42]  S. Yeh,et al.  Targeting androgen receptor leads to suppression of prostate cancer via induction of autophagy. , 2012, The Journal of urology.

[43]  C. Sander,et al.  Integrative genomic profiling of human prostate cancer. , 2010, Cancer cell.

[44]  J. Humm,et al.  Antitumour activity of MDV3100 in castration-resistant prostate cancer: a phase 1–2 study , 2010, The Lancet.

[45]  C. Giacomantonio,et al.  Curcumin-Induced Apoptosis in PC3 Prostate Carcinoma Cells Is Caspase-Independent and Involves Cellular Ceramide Accumulation and Damage to Mitochondria , 2010, Nutrition and cancer.

[46]  Matthew R. Thompson,et al.  ATF3 transcription factor and its emerging roles in immunity and cancer , 2009, Journal of Molecular Medicine.

[47]  Xia Li,et al.  KLF6 Induces Apoptosis in Prostate Cancer Cells through Up-regulation of ATF3* , 2008, Journal of Biological Chemistry.

[48]  M. McArthur,et al.  The transcription factor ATF3 acts as an oncogene in mouse mammary tumorigenesis , 2008, BMC Cancer.

[49]  M. Becich,et al.  Gene expression profiles of prostate cancer reveal involvement of multiple molecular pathways in the metastatic process , 2007, BMC Cancer.

[50]  H. Klocker,et al.  The expression of transcription factor activating transcription factor 3 in the human prostate and its regulation by androgen in prostate cancer. , 2006, The Journal of urology.

[51]  John T. Wei,et al.  Integrative genomic and proteomic analysis of prostate cancer reveals signatures of metastatic progression. , 2005, Cancer cell.

[52]  John M Sedivy,et al.  Stress response gene ATF3 is a target of c‐myc in serum‐induced cell proliferation , 2005, The EMBO journal.

[53]  D. Grigoryev,et al.  Simvastatin attenuates vascular leak and inflammation in murine inflammatory lung injury. , 2005, American journal of physiology. Lung cellular and molecular physiology.

[54]  C. Huggins,et al.  Studies on prostatic cancer. I. The effect of castration, of estrogen and androgen injection on serum phosphatases in metastatic carcinoma of the prostate. , 1941, CA: a cancer journal for clinicians.

[55]  H. Kung,et al.  ASC-J9 suppresses castration-resistant prostate cancer growth through degradation of full-length and splice variant androgen receptors. , 2012, Neoplasia.

[56]  Kedar S Vaidya,et al.  Metastasis suppressors genes in cancer. , 2008, The international journal of biochemistry & cell biology.

[57]  John T. Wei,et al.  Integrative molecular concept modeling of prostate cancer progression , 2007, Nature Genetics.

[58]  C. Logothetis,et al.  Osteoblasts in prostate cancer metastasis to bone , 2005, Nature Reviews Cancer.

[59]  N. Dubrawsky.  Cancer statistics , 1989, CA: a cancer journal for clinicians.