PPP2R2A overexpression rescues the miR-21–induced biological effects in bladder cancer cells. PPP2R2A overexpression rescues the miR-21–induced biological.

Slides:



Advertisements
Similar presentations
Volume 133, Issue 1, Pages (July 2007)
Advertisements

Figure 1. Herbacetin binds to AKT1/2 and suppresses each respective kinase activity. The effect of herbacetin on (A) PI3K/AKT and (B) MAPK signaling pathway.
Molecular Therapy - Oncolytics
Figure 1. Herbacetin binds to AKT1/2 and suppresses each respective kinase activity. The effect of herbacetin on (A) PI3K/AKT and (B) MAPK signaling pathway.
SCC244 significantly inhibited c-Met–driven tumor growth in cancer CDX models. SCC244 significantly inhibited c-Met–driven tumor growth in cancer CDX models.
Inhibition of FGFR fusion kinase activity repressed tumor growth in a mouse xenograft model. Inhibition of FGFR fusion kinase activity repressed tumor.
miR-133a positively regulated p53/p21 pathway.
The TCL1 oncoprotein inhibits activation-induced cell death by impairing PKCθ and ERK pathways by Gilles Despouy, Marjorie Joiner, Emilie Le Toriellec,
Volume 133, Issue 1, Pages (July 2007)
Nod2-Induced Autocrine Interleukin-1 Alters Signaling by ERK and p38 to Differentially Regulate Secretion of Inflammatory Cytokines  Matija Hedl, Clara.
Teruaki Fujishita, Masahiro Aoki, Makoto M. Taketo  Gastroenterology 
Arachidonic acid regulation of the cytosolic phospholipase A2α/cyclooxygenase-2 pathway in mouse endometrial stromal cells  Zhen-Ao Zhao, Ph.D., Zhi-Rong.
Effects of SC144 on in vivo ovarian tumor.
Identification of TLOC1 and SKIL as tumor driver genes in 3q26.
NF1 downregulation activates MAPK pathway signaling.
A, left: indicated MEFs were transfected as described in the Methods section. A, left: indicated MEFs were transfected as described in the Methods section.
Downregulation of SPRY4 expression is associated with FGFR1–FRS2 activation. Downregulation of SPRY4 expression is associated with FGFR1–FRS2 activation.
Knockdown of DAO inhibits DNA damage–induced senescence.
PI(3,4,5)P3 releases SIN1-PH–mediated inhibition on mTOR-KD, leading to mTORC2 activation. PI(3,4,5)P3 releases SIN1-PH–mediated inhibition on mTOR-KD,
Volume 50, Issue 2, Pages (April 2013)
AMPK induces VEGF-A production by upregulating ERK signaling.
Mst1 Is an Interacting Protein that Mediates PHLPPs' Induced Apoptosis
eIF5A-PEAK1 signaling regulates KRAS protein expression.
Lapatinib reduces IGF-I signaling in trastuzumab-resistant cells.
P38 activation mediates chronic insulin-induced IRS1 and IRS2 degradation and is involved in myocardial insulin resistance in vitro. p38 activation mediates.
USP2a regulates MYC expression through the MDM2–p53 axis.
JAK3A572V mutation causes constitutive JAK3 activity and IL-2–independent proliferation of NKTCL cells. JAK3A572V mutation causes constitutive JAK3 activity.
CREB1 promotes the induction of endogenous ERα target genes.
Monitoring perturbation of ER-mitochondria interactions linked to genetic modulation of protein of the VDAC1/Grp75/IP3R1 complex by in situ PLA. Representative.
Induction of apoptosis by NMT siRNAs.
Aβ-mediated Ras-MAPK signaling and Cyclin D1 expression in B103 cells are dependent on APP expression and can be reversed with MEK or Ras inhibition. Aβ-mediated.
OPCML-associated RTK modulation affects downstream signaling.
GR cells are dependent upon sustained CDC25C signaling as pharmacologic or genetic inhibition of CDC25C induce synthetic lethality. GR cells are dependent.
Gramicidin A (GA) decreases HIF protein expression in RCC cells.
PTENP1 serves as a ceRNA in the regulation of tumor growth in RCC
PTENP1 sensitizes renal cancer cells to chemotherapy.
Effect of LY on phosphorylation of various MAP kinase substrates in HeLa cells in vitro. Effect of LY on phosphorylation of various MAP kinase.
Molecular Therapy - Oncolytics
TSA-mediated changes in cell cycle inhibitor proteins.
Overexpression of miR-335, but not miR-29a, reduces in vitro carcinogenesis. Overexpression of miR-335, but not miR-29a, reduces in vitro carcinogenesis.
Depletion of HDAC2 sensitizes cells to epirubicin-induced apoptosis.
Correlation of miR-21 expression levels with DEGs in 28 bladder cancer cell lines. Correlation of miR-21 expression levels with DEGs in 28 bladder cancer.
Effect of other nucleoside analogues on p38 MAPK phosphorylation levels. Effect of other nucleoside analogues on p38 MAPK phosphorylation levels. A, MM.1S.
Angiogenesis in tumors formed by cells varying in the expression of CXCR2. Angiogenesis in tumors formed by cells varying in the expression of CXCR2. A,
In vivo tumorigenicity of MKN-1 cells with sustained suppression of HDAC2. In vivo tumorigenicity of MKN-1 cells with sustained suppression of HDAC2. A,
Src expression in a panel of human TCC cell lines.
Colony formation of K-562 cells after 24 h (upper panel) or 48 h (lower panel) exposure to ErPC3 (20 μm) and ASO-bcr (10 μm), respectively. Colony formation.
Effect of miRNA mimic on platinum sensitivity.
ERK reactivation following EGFR TKI treatment.
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.
CLIC1 supports invadopodia formation in vitro and metastasis in vivo.
SBC-5 miR-335+, but not SBC-5 miR-29a+, exhibited reduced IGF-IR expression. SBC-5 miR-335+, but not SBC-5 miR-29a+, exhibited reduced IGF-IR expression.
miR-100 suppresses bladder cancer cell growth in vitro and in vivo.
The effects of HDAC2 knockdown on cell-cycle proteins.
Changes in signal transduction pathway induced by gefitinib.
NT157 treatment inhibits LNCaP xenograft growth and delays castration-resistant progression. NT157 treatment inhibits LNCaP xenograft growth and delays.
Activity of a chemically modified miR-21 inhibitor in human bladder cancer xenografts. Activity of a chemically modified miR-21 inhibitor in human bladder.
HES1-dependent activation of SRC/STAT3 pathway is mediated by transcription-independent mechanism. HES1-dependent activation of SRC/STAT3 pathway is mediated.
RUNX3 depletion induces cellular senescence and inflammatory cytokine expression in cells undergoing TGFβ-mediated EMT. A, Cells were transfected with.
EMT alters activation of AKT and serum-independent proliferation.
PVT1 facilitated gastric cancer progression in a FOXM1-mediated manner
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.
DEAR1 blocks TGF-β–induced anoikis resistance, and TGF-β and SMAD3 signal transduction. DEAR1 blocks TGF-β–induced anoikis resistance, and TGF-β and SMAD3.
AXL overexpression decreases proliferation in vitro.
p53β regulates cellular senescence.
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.
FGFR2 amplification in primary human gastric tumors predicts for response to NVP-BGJ398. FGFR2 amplification in primary human gastric tumors predicts for.
T3 or T4 induces MAPK activation in myeloma cells.
AXL is not necessary for maintenance of intrinsic resistance.
D-GM3 promotes uPAR clustering on the cell surface and activates p38 MAPK. A, uPAR expression in cells was either knocked down by treatment with 4 independent.
Presentation transcript:

PPP2R2A overexpression rescues the miR-21–induced biological effects in bladder cancer cells. PPP2R2A overexpression rescues the miR-21–induced biological effects in bladder cancer cells. IB for phosphorylated p44/p42 MAPK (Thr202/Tyr204) and total-p44/p42 MAPK in (A) bladder cancer cells and (B) excised tumors originating from 5637 bearing mouse xenografts, after treatment with 50 nmol/L LNA miR-21 or MKAD-21 (20 mg/kg) and the respective scramble controls. C, The effect of PPP2R2A enforced expression on ERK pathway activation in miR-21 mimic- or mimic miR-scr–treated, serum-starved, and FBS-stimulated bladder cancer cells, as assessed by IB analysis. Cell treatment with 100 nmol/L mimic miR-scr or miR-21 mimic was followed by transient transfection of pPM-C-His vector or Blank-Control Protein Vector. D, Dynamic monitoring of bladder cancer cellular proliferation upon miR-21 and PPP2R2A parallel overexpression, using the xCELLigence RTCA SP system. E, PPP2R2A overexpression causes reversal of miR-21–mediated induction of the colony formation ability of RT-112 cells. Representative images of colonies are shown in the top panel and the respective quantification in the bottom plot. Mimic miR-scr+empty vector, cells treated with 100 nmol/L mimic miR-scr for 24 hours followed by transfection with Blank-Control Protein Vector; Mimic miR-scr+PPP2R2A vector, cells treated with 100 nmol/L mimic miR-scr for 24 hours followed by transfection with pPM-C-His vector; miR-21 mimic+empty vector, cells treated with 100 nmol/L mimic miR-21 for 24 hours followed by transfection with Blank-Control Protein Vector; miR-21 mimic+PPP2R2A vector, cells treated with 100 nmol/L mimic miR-21 for 24 hours followed by transfection with pPM-C-His vector. Data are shown as the mean ± SE. Asterisks denote statistical significant differences: *, P < 0.05 and ***, P < 0.001. Marina Koutsioumpa et al. Mol Cancer Ther 2018;17:1430-1440 ©2018 by American Association for Cancer Research