EMT alters activation of AKT and serum-independent proliferation.

Slides:



Advertisements
Similar presentations
Date of download: 6/22/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Hyaluronan and the Interaction Between CD44 and Epidermal.
Advertisements

PI 3-kinase inhibition has no effect on ANG II induced extracellular recognition kinase (ERK) 1/2 activation. PI 3-kinase inhibition has no effect on ANG.
Copyright © 2010 American Medical Association. All rights reserved.
From: IGF-1 Regulates the Extracellular Level of Active MMP-2 and Promotes Müller Glial Cell Motility Invest. Ophthalmol. Vis. Sci ;56(11):
HER2 mutations V777L, D769H, V842I, G309A induce gain-of-function over HER2 WT in MCF10A mammary epithelial cells. HER2 mutations V777L, D769H, V842I,
Inhibition of PDGFR-β downstream signaling events by flavones.
Nicotine Induces Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor by α1 Nicotinic Acetylcholine Receptor–Mediated Activation in.
The cyclolignan picropodophyllin attenuates intimal hyperplasia after rat carotid balloon injury by blocking insulin-like growth factor-1 receptor signaling 
Relationship between adhesion plaque formation, FAK/ERK signaling, and proliferation. Relationship between adhesion plaque formation, FAK/ERK signaling,
by Xingwei Sui, Sanford B. Krantz, Min You, and Zhizhuang Zhao
Identification of a MEK2 mutation in a melanoma sample resistant to dabrafenib/trametinib. Identification of a MEK2 mutation in a melanoma sample resistant.
Volume 67, Issue 6, Pages (June 2005)
Nicotine Induces Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor by α1 Nicotinic Acetylcholine Receptor–Mediated Activation in.
PDK1 regulates PLK1 in vivo and in vitro.
Bortezomib sensitivity correlates with basal NF-κB activity in KP lung adenocarcinoma cell lines. Bortezomib sensitivity correlates with basal NF-κB activity.
NF1 downregulation activates MAPK pathway signaling.
nab-Paclitaxel targets the tumor epithelial cells.
The EGF receptor confers BRAF inhibitor resistance in BRAF-mutant melanoma cells. The EGF receptor confers BRAF inhibitor resistance in BRAF-mutant melanoma.
The selective PI3K inhibitor A66 suppresses PIP3 accumulation, AKT phosphorylation at Thr308, and YAP/TAZ–regulated gene expression in PDAC cells. The.
AMPK induces VEGF-A production by upregulating ERK signaling.
The role of SRC-C3G-RAP1 signaling in transformation induced by CRKL
AKT2, but not AKT1, is required for regulating survival of PTEN-deficient prostate tumor spheroids. AKT2, but not AKT1, is required for regulating survival.
TDP1 knockdown increases the sensitivity of rhabdomyosarcoma cell lines to CPT treatment. TDP1 knockdown increases the sensitivity of rhabdomyosarcoma.
CEP55 is a downstream effector of MAPK signaling
Involvement of Activin/Nodal, PI3-kinase and MAPK signaling pathways in β-catenin-induced mesoderm and the anterior PS differentiation. Involvement of.
Lapatinib reduces IGF-I signaling in trastuzumab-resistant cells.
JAK3A572V mutation causes constitutive JAK3 activity and IL-2–independent proliferation of NKTCL cells. JAK3A572V mutation causes constitutive JAK3 activity.
Synergistic interaction of Activin and canonical Wnt/β-catenin signaling pathways in the anterior PS/endoderm specification during hES cell differentiation.
CML-HSA treatment activates MAPK family members ERK1/2 and p38 but not JNK. Samples were taken at the indicated times after 100 μg/ml CML-HSA exposure.
The dynamics of Akt activation in cultured human keratinocytes.
BCR–ABL kinase activity rewires GM-CSFR signaling and confers oncogene addiction in TF1 cells. BCR–ABL kinase activity rewires GM-CSFR signaling and confers.
PKM2 is tyrosine phosphorylated and inhibited by FGFR1 in cancer cells with oncogenic or overexpressed FGFR1. PKM2 is tyrosine phosphorylated and inhibited.
Peripheral CAF model. Peripheral CAF model. A, bright field (top) and fluorescence (bottom) micrographs of aggregates that contain RFP-tagged 344SQ cells.
G3139 substitutes for heparin, which is required for the biological activity of FGF2. G3139 substitutes for heparin, which is required for the biological.
Effect of LY on phosphorylation of various MAP kinase substrates in HeLa cells in vitro. Effect of LY on phosphorylation of various MAP kinase.
Suppression of melanoma cell proliferation in response to kinase inhibitors. Suppression of melanoma cell proliferation in response to kinase inhibitors.
TGF-β1 modulates extracellular matrix–mediated MT1-MMP expression.
Down-regulation of the erbB-2 receptor by trastuzumab decreases Akt kinase activation but not MAPK activation. Down-regulation of the erbB-2 receptor by.
Effects of visfatin on the cell proliferation and phosphorylation of ERK, Akt, and GSK-3β proteins in HCC cells. Effects of visfatin on the cell proliferation.
Drug sensitivities of IGROV1 cells to AGF94 and PMX at leucovorin (LCV) concentrations of 2 and 25 nmol/L. Drug sensitivities of IGROV1 cells to AGF94.
MiR-200c is a PI3K–AKT signaling pathway regulator in CRC
The effect of IAA and glycyrrhizin (Gc) on growth of human melanoma cells. The effect of IAA and glycyrrhizin (Gc) on growth of human melanoma cells. A,
A. A. Honokiol inhibits TNF-induced NF-κB activation, IκBα phosphorylation, and IκBα degradation. Honokiol inhibits TNF-induced activation of NF-κB. H1299.
MDA-468TR-PTEN (with and without 100 ng/ml doxycycline) and MDA-468TR-vector (with dox) were serum starved overnight and the following day treated for.
PPP2R2A overexpression rescues the miR-21–induced biological effects in bladder cancer cells. PPP2R2A overexpression rescues the miR-21–induced biological.
Inhibition of EGFR kinase activity and autophosphorylation by Iressa.
Synergistic cytotoxicity of 17AAG and TNF treatment in human lung cancer cell lines. Synergistic cytotoxicity of 17AAG and TNF treatment in human lung.
ERK reactivation following EGFR TKI treatment.
The effect of different concentrations of WMC-79 and time of exposure on the growth of HCT-116 cells. The effect of different concentrations of WMC-79.
Induction of DNA strand breaks by artesunate.
PKCζ is tyrosine phosphorylated by EGF and contributes to EGF-induced activation of ERK in Mef cells. PKCζ is tyrosine phosphorylated by EGF and contributes.
Expression of dominant-negative RasN17 completely suppresses Ras activation in Rh1 cells. Expression of dominant-negative RasN17 completely suppresses.
Changes in signal transduction pathway induced by gefitinib.
A combination of neurotensin and insulin potently decreases YAP phosphorylation at Ser127 and Ser397 in PDAC cells. A combination of neurotensin and insulin.
The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. Serum-starved.
Knockdown of ERBB3, NRG1, or ERBB2 in H358-TwistER cells reduces basal PI3K–AKT signaling and ablates serum-independent proliferation before EMT. A and.
Effect of NO and eNOS on prostate cancer cell growth.
Wnt5A decreases ROR1 expression through proteasomal degradation.
A, cell number was assessed 96 hours after exposure to indicated treatment in indicated cell models. A, cell number was assessed 96 hours after exposure.
EGCG affects growth factor receptor signaling in H2111, H358, and H460 NSCLC cells. EGCG affects growth factor receptor signaling in H2111, H358, and H460.
AKT activation in HCC2429 is SRC- but not Notch-dependent.
Proliferation of TA3-Ha and TA3-St cells in vitro and in vivo.
Heterogeneous resistance mechanisms develop in response to W+T combination treatment in the EGFRL858R/T790M genetically engineered mice. Heterogeneous.
Identification of the molecular regulators of FLP formation.
PLK1 is a crucial downstream effector of PDK1 for MYC activation and cell survival. PLK1 is a crucial downstream effector of PDK1 for MYC activation and.
EPHA2 inhibitors inhibit phosphorylation of AKT and ERK, arrest cell cycle at G0–G1, and induce apoptosis in both vemurafenib (VEM)-sensitive and VEM-resistant.
NVP-BGJ398 inhibits proliferation of a subset of cancer cell lines.
Inhibition of BCR-mediated signaling by ARQ 531.
MET activation confers resistance to cetuximab (Cmab) or panitumumab (Pmab) in colon cancer cell lines in vitro and in vivo. MET activation confers resistance.
AXL is not necessary for maintenance of intrinsic resistance.
Presentation transcript:

EMT alters activation of AKT and serum-independent proliferation. EMT alters activation of AKT and serum-independent proliferation. A, H358-TwistER– and H358-SnailER–expressing cells cultured over 15 days with 100 nmol/L 4-hydroxytamoxifen (4OHT). B, basal phosphorylation (p) of AKT (S473), AKT effectors, and extracellular signal-regulated kinase (ERK) in H358-TwistER and H358-SnailER cells before (NT) and after (4OHT) 14 days of 4OHT treatment with (10%) or without (SS, serum starved) serum overnight. C and D, proliferation of untreated (top) or 4OHT-pretreated (bottom) H358-TwistER and H358-SnailER cells in the presence (10%) or absence (SS) of serum. Error bars represent SD. Megan B. Salt et al. Cancer Discovery 2014;4:186-199 ©2014 by American Association for Cancer Research