PKIs block DHT + bombesin-induced transactivation of probasin ARR3 tk-luc and PSA pPUE-E1b-Luc report constructs. PKIs block DHT + bombesin-induced transactivation.

Slides:



Advertisements
Similar presentations
Date of download: 9/17/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Differential Responses of Human Papillary Thyroid.
Advertisements

Figure 1. Schematic location of the amino acid substitutions and truncations of the androgen receptor. NTD, N-terminal domain; DBD, DNA binding domain;
Copyright © 2007 American Medical Association. All rights reserved.
KG-501 suppresses NSCLC/IL-1β CM–induced migration of HUVECs by regulating IL-1β–induced CXC chemokine gene expression in NSCLC cells. KG-501 suppresses.
IL-1β significantly augments the angiogenic activity of NSCLC by inducing the expression of angiogenic CXC chemokine genes. IL-1β significantly augments.
IL-1β differentially regulates CXCL5 and CXCL8 protein secretion in NHTBE and NSCLC cells. IL-1β differentially regulates CXCL5 and CXCL8 protein secretion.
IL-1β stimulates CXCL5 and CXCL8 gene expression and protein secretion in A549 cells in a time- and dose-dependent manner. IL-1β stimulates CXCL5 and CXCL8.
EP4 promoter activity is induced by sulindac sulfide in T98G cells.
Volume 16, Issue 4, Pages (October 2009)
Suppressive effect of CD39+CD73+ melanoma cells on T-cell proliferation, and reversion of this effect via treatment with the CD39-blocking antibody, CD39.
COX-2–PGE2 signaling is required for MSC-induced increase in ALDHhigh CSC-enriched population and tumor initiation. COX-2–PGE2 signaling is required for.
Volume 116, Issue 6, Pages (June 1999)
Allopurinol up-regulates DR5 expression in PC-3 and DU145 cells.
SW fraction induces S phase arrest and apoptosis.
Association of NM-HA and NM-GFP with SGs is transient.
Curcumin-generated ROS activates Chk1 and Chk2 kinases.
Cell viability assay and expression of COX protein.
PX-478 inhibits hypoxic HIF-1 protein expression and signaling activity in a dose-dependent manner. PX-478 inhibits hypoxic HIF-1 protein expression and.
VP16-E2 is a more potent transcriptional activator than Gal4-VP16.
Gramicidin A (GA) decreases HIF protein expression in RCC cells.
B7-H1–induced reverse signals in myeloma cells.
T-VISA is robust in ovarian cancer cell lines.
Silencing hOGG1 triggers caspase-3 and caspase-7 activation in response to H2O2 in GM00637 cells. Silencing hOGG1 triggers caspase-3 and caspase-7 activation.
Dietary plant extracts inhibit NF-κB activation in vitro.
Suppression of melanoma cell proliferation in response to kinase inhibitors. Suppression of melanoma cell proliferation in response to kinase inhibitors.
CDDO-Me induces apoptosis independent of Bcl-2 level as well as p53 status in human NSCLC cells. CDDO-Me induces apoptosis independent of Bcl-2 level as.
Protein expression profile in a dasatinib-resistant cell line.
Dephosphorylation of pocket proteins in response to AG1024.
Effect of anti-CYP3A and anti-CYP2C antibodies on the disappearance of MPA in human liver microsomes (GHL24). Effect of anti-CYP3A and anti-CYP2C antibodies.
Binding and internalization of bispecific immunotoxins.
Reconstitution of RhoH expression in HCL inhibits homotypic adhesion.
Immunohistochemistry for phosphorylated (S235) S6 ribosomal protein and quantitation of Ki67 labeling indices in vehicle- and WAY –treated Eker (Tsc2+/−)
Overexpression of EP4 with cAMP-PKA signal activation promoted the castration-resistant progression of LNCaP cells through AR activation. Overexpression.
N-3 PUFAs promote endometrial cancer cell apoptosis in vitro and in vivo. n-3 PUFAs promote endometrial cancer cell apoptosis in vitro and in vivo. HEC-1-A.
Cocultivation of fibroblasts with epithelial cells (EP156T-luc).
Tipifarnib combined with bortezomib induces cell death in diverse multiple myeloma and AML cell lines. Tipifarnib combined with bortezomib induces cell.
Bone marrow stroma partially protects multiple myeloma and AML cell lines from tipifarnib- and bortezomib-induced cell death. 8226/S myeloma cells were.
Time course of a G2-M arrest in response to 6-TG compared with IR and VP-16, showing that 6-TG induced a delayed G2-M arrest in MMR+ cells. Time course.
Incorporation of the TSTA system into a single plasmid.
Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. LNCaP,
Combined inhibition of Wee1 and PARP causes persistent radiation-induced DNA damage. Combined inhibition of Wee1 and PARP causes persistent radiation-induced.
A and B, comparison of time course of TFF1 mRNA induction under estrogen-withdrawn (denoted ph−/ES−) and estrogenic medium (denoted ph+/ES+) conditions.
Carcinoma cell–secreted IL-1 induces PGE2 production in MSCs
Effect of NO and eNOS on prostate cancer cell growth.
MAPK/ERK signaling regulates TLR4 gene expression in response to BRAFV600E. MAPK/ERK signaling regulates TLR4 gene expression in response to BRAFV600E.
Pdcd4 expression inhibits AP-1 transactivation.
A, capsid modifications increase the infectivity of gastric cancer cell lines. A, capsid modifications increase the infectivity of gastric cancer cell.
Induction of apoptosis by statins in NB4 cells and NB4 variant cell lines. Induction of apoptosis by statins in NB4 cells and NB4 variant cell lines. A,
Enhanced expression of Cap43 gene by nickel in breast cancer cell lines. Enhanced expression of Cap43 gene by nickel in breast cancer cell lines. Expression.
AS1411 alters subcellular distribution of PRMT5 in a time-dependent, dose-dependent, and nucleolin-dependent manner. AS1411 alters subcellular distribution.
SAHA blocks IR-induced increase of RAD51 protein in MM cells.
The effects of AZD1775 and olaparib on DNA damage response signaling.
BCR/ABL expression, tyrosine phosphorylation, and signaling in dasatinib- and imatinib-resistant cell lines and the ubiquitin inhibitor lactacystin modifies.
Inhibitory effects of nobiletin and luteolin on TPA-induced O2− generation in differentiated HL-60 cells and their cellular uptake. Inhibitory effects.
Functional SLC6A3 in ccRCC cell lines KMRC3 and SNU-349, but not in conventional cell lines. Functional SLC6A3 in ccRCC cell lines KMRC3 and SNU-349, but.
Effect of bevacizumab on the proliferation of A2780 cells.
CpG oligodeoxynucleotide (CpG ODN)–induced activation of different types of primary malignant B cells. CpG oligodeoxynucleotide (CpG ODN)–induced activation.
Effects of W. chinensis extract on androgen activity and growth of prostate cancer cells. Effects of W. chinensis extract on androgen activity and growth.
Effects of ZOL treatment on pulmonary metastases.
Effect of dexamethasone on PCDGF/GP88 mRNA and protein expressions and effect of PCDGF/GP88 on dexamethasone-induced cell death. Effect of dexamethasone.
Expression of chemokine receptors in A-498 cell line.
Relative frequencies of FGFR aberrations in non–small cell lung carcinoma. Relative frequencies of FGFR aberrations in non–small cell lung carcinoma. A,
Blockade of cell cycle at G2-M phase in Bel-7402 cells treated with IG-105. Blockade of cell cycle at G2-M phase in Bel-7402 cells treated with IG-105.
IL-1β expression is increased in MM cell lines by the co-culture with platelets in vitro. IL-1β expression is increased in MM cell lines by the co-culture.
Mechanism by which flavopiridol induces cell cycle arrest and apoptosis in rhabdoid tumor cells. Mechanism by which flavopiridol induces cell cycle arrest.
MTOR kinase inhibition–induced reactivation of AKT substrates is HER2 and PI3K dependent. mTOR kinase inhibition–induced reactivation of AKT substrates.
Induction of PD-1 in B cells by TLR agonists and primary HCC-SN.
Curcumin decreases viability and proliferation of Bcr-Abl-expressing cells. Curcumin decreases viability and proliferation of Bcr-Abl-expressing cells.
Effect of SFN on the total activity and protein expression of HDACs in JB6 P+ cells. Effect of SFN on the total activity and protein expression of HDACs.
Effects of inhibitors of PI3K, MEK1, and GSK-3β on visfatin-induced proliferation in HepG2 cells. Effects of inhibitors of PI3K, MEK1, and GSK-3β on visfatin-induced.
Presentation transcript:

PKIs block DHT + bombesin-induced transactivation of probasin ARR3 tk-luc and PSA pPUE-E1b-Luc report constructs. PKIs block DHT + bombesin-induced transactivation of probasin ARR3 tk-luc and PSA pPUE-E1b-Luc report constructs. PC-3 cells were treated as indicated in Fig. 1<$REFLINK> legend and incubated with medium containing the following: column pair 1, medium only (Control); column pair 2, 10 pm DHT (DHT); column pair 3, 5 nm bombesin (Bomb); column pair 4, DHT + bombesin (DHT+Bomb); column pair 5, 10 μm PKI (PKI); column pair 6, 10 μm MAP kinase inhibitor PD 98059 (PD 98059); column pair 7, 10 μm protein kinase C inhibitor GF-109203X (GF-109203X); column pair 8, DHT + bombesin + PKI (DHT +Bomb+PKI); column pair 9, DHT + bombesin + PD 98059 (DHT+Bomb+PD); column pair 10, DHT + bombesin + GF-109203X (DHT+Bomb+GF); column pair 11, DHT + bombesin + protein kinase inhibitors mixture (DHT+Bomb+Mix). Cells were pretreated for 1 h with inhibitors and then incubated in medium containing bombesin and DHT for 24 h, and luciferase activities were measured. Results are expressed as the relative percentage of activity, with the values resulting from DHT + bombesin set to 100%. Mean values were calculated from three independent experiments performed in duplicate; bars, SE. Jie Dai et al. Clin Cancer Res 2002;8:2399-2405 ©2002 by American Association for Cancer Research