Reduction of Sca-1 increases PPARγ expression.

Slides:

Advertisements

Similar presentations

Adipose PancreasAorta MuscleHeart Liver LungKidney Testis Spleen Brian 18S p55 γ p55 α Figure S1 Tissue distribution of p55 . (A) Representative RT-PCR.

Advertisements

Phosphatidylinositol 3-Kinase and Calcium-Activated Transcription Pathways Are Required for VLDL-Induced Smooth Muscle Cell Proliferation by Larissa Lipskaia,

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.

PI3K isoform–selective inhibitors and PTEN induction decrease ERK phosphorylation. PI3K isoform–selective inhibitors and PTEN induction decrease ERK phosphorylation.

Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.

25(OH)D and 1,25(OH)2D perfusion treatment effect on cancer-related markers: IF stains illustrating expression levels for Ki-67 (A), cyclin D1 (B), ErbB-2.

Volume 8, Issue 5, Pages (September 2014)

NRP2 represses IGF-IR expression and signaling.

Pioglitazone inhibits aromatase expression in human preadipocytes.

CHK1 downregulation upon ERG overexpression.

The EGF receptor confers BRAF inhibitor resistance in BRAF-mutant melanoma cells. The EGF receptor confers BRAF inhibitor resistance in BRAF-mutant melanoma.

Collagen-dependent phosphorylation of eIF4E in PDAC cells.

p38 MAPK activation is required for phosphorylation of Akt at Ser473.

Pharmacologic inhibition of eIF5A hypusination sensitizes KRas-driven tumor cells to MEK and KRas inhibition. Pharmacologic inhibition of eIF5A hypusination.

HIPK2 decreases the stability of Notch1-IC through proteasome-dependent degradation. HIPK2 decreases the stability of Notch1-IC through proteasome-dependent.

Expression changes of specific epigenetic-controlled tumor-related genes by the prenatal/maternal BSp treatment. qRT-PCR and Western blot analysis were.

eIF5A-PEAK1 signaling regulates KRAS protein expression.

Knocking down Wnt3 increases the cells' response to trastuzumab and reduces cells' invasiveness. Knocking down Wnt3 increases the cells' response to trastuzumab.

Figure 4 DNM1 mutations affect protein levels and self-dimerization (A) HeLa cells were transfected with green fluorescent protein (GFP)-tagged mutant.

Mechanism of Akt1 in promoting reprogramming.

SIRT1 is downregulated in human gastric cancer (GC).

PTK6 downregulation suppresses SNAIL and increases E-cadherin expression. PTK6 downregulation suppresses SNAIL and increases E-cadherin expression. A,

Class 1 phosphatidylinositol 3-kinase (PI3K) p85 subunit dominant negative adenovirus regulates Pax2 and GAPDH abundance in NRK-52E cells. Class 1 phosphatidylinositol.

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.

Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.

TFAP2A is highly expressed in nasopharyngeal carcinoma cells and tumor tissues. TFAP2A is highly expressed in nasopharyngeal carcinoma cells and tumor.

Activating mutation of Ras is associated with CDCP1 expression in NSCLC. A, NSCLC cell lines with Ras + B-Raf mutations and wild-type Ras were examined.

Increased CCL5 expression, infiltration of Treg cells, and apoptosis of CD8+ T cells in human colorectal tissues. Increased CCL5 expression, infiltration.

The role of p53 in H2O2-mediated cell death of hOGG1-deficient H1299 lung carcinoma p53 null cells. The role of p53 in H2O2-mediated cell death of hOGG1-deficient.

Imatinib mesylate inhibits PDGF-mediated ERK and Akt activation.

ALDH1A3 is mainly responsible for the ALDH activity in two human cholangiocarcinoma lines. ALDH1A3 is mainly responsible for the ALDH activity in two human.

Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. A.

The effect of IAA on tumor growth in an SK-MEL-28 xenograft model.

The effects of IAA and glycyrrhizin (Gc) on proliferation and cell-cycle distribution. The effects of IAA and glycyrrhizin (Gc) on proliferation and cell-cycle.

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.

Western blot analysis of Wnt signaling genes.

PTEN expression regulates autophagy in tumor cells, reducing T cell–mediated killing. PTEN expression regulates autophagy in tumor cells, reducing T cell–mediated.

A. A. Honokiol inhibits TNF-induced NF-κB activation, IκBα phosphorylation, and IκBα degradation. Honokiol inhibits TNF-induced activation of NF-κB. H1299.

Effect of SFN on the protein expression of Nrf2, HO-1, and NQO1 in JB6-shMock and JB6-shNrf2 cells. Effect of SFN on the protein expression of Nrf2, HO-1,

TFAP2A knockdown inhibits cell growth by targeting HIF-1α signaling.

IAA inhibits PI3K, MKK4, and MKK7 kinase activities by directly binding in an ATP-competitive manner. IAA inhibits PI3K, MKK4, and MKK7 kinase activities.

Expression pattern of TLR-4 and MyD88 in EOC cells.

Activation of mTOR signaling (increased phosphorylated S6 ribosomal protein) and loss of inhibition of IRS-1 in human endometrial carcinomas. Activation.

Dysregulated NF-κB activation in Il1r8+/+/lpr and Il1r8−/−/lpr mice.

COX-2, Oct-4, and ALDH-1 expression in the mammary gland.

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.

Changes in signal transduction pathway induced by gefitinib.

Met is expressed in Her2-overexpressing cell lines and Her2 (+) breast tumors. Met is expressed in Her2-overexpressing cell lines and Her2 (+) breast tumors.

Tivantinib does not inhibit MET function.

The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. Serum-starved.

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.

Γ-TmT reduces serum E2 levels and induces estrogen-metabolizing enzyme CYP1A1 in E2-treated ACI rats. γ-TmT reduces serum E2 levels and induces estrogen-metabolizing.

AS1411 alters subcellular distribution of PRMT5 in a time-dependent, dose-dependent, and nucleolin-dependent manner. AS1411 alters subcellular distribution.

Cell-cycle regulatory proteins were controlled by O-GlcNAc at FOXO3 S284 through MDM2. Cell-cycle regulatory proteins were controlled by O-GlcNAc at FOXO3.

BCR/ABL expression, tyrosine phosphorylation, and signaling in dasatinib- and imatinib-resistant cell lines and the ubiquitin inhibitor lactacystin modifies.

EGCG affects growth factor receptor signaling in H2111, H358, and H460 NSCLC cells. EGCG affects growth factor receptor signaling in H2111, H358, and H460.

Effect of bevacizumab on the proliferation of A2780 cells.

TGFβ1/Smad3 signaling suppresses IFNγ production via an E4BP4-dependent mechanism in NK-92 cells. TGFβ1/Smad3 signaling suppresses IFNγ production via.

Expression and induction of HER2 and HPSE in 231BMBC cells.

ER stress mediates postslippage AMPK activation.

Increased growth factor receptor expression in lungs and tumors of hypoxic mice. Increased growth factor receptor expression in lungs and tumors of hypoxic.

PARP1 suppresses the transcription of PD-L1 in cancer cells.

Effect of dexamethasone on PCDGF/GP88 mRNA and protein expressions and effect of PCDGF/GP88 on dexamethasone-induced cell death. Effect of dexamethasone.

Quercetin induces autophagy, blocks cell cycle and activation of ERK and JNK signaling pathways participates in the G1 arrest in P39 cells. Quercetin induces.

FGF19 amplification in liver cancer cell lines is associated with response to NVP-BGJ398. FGF19 amplification in liver cancer cell lines is associated.

Coculture with U937 cells enhances DNMT1 expression in gastric cancer cells. Coculture with U937 cells enhances DNMT1 expression in gastric cancer 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.

Inhibition of HDACs disrupts DNMT1 association with Hsp90.

PD-L1 expression is not associated with PTEN expression status in melanomas. PD-L1 expression is not associated with PTEN expression status in melanomas.

Determination of Per2 (left), MTNR1A (middle), and ERβ (right) protein expression levels in mammary tissues of rats sacrificed at ZT12. Determination of.

Presentation transcript:

Reduction of Sca-1 increases PPARγ expression. Reduction of Sca-1 increases PPARγ expression. A, 34T mammary tumor cells were transduced with either a GFP shRNA (34T) or a Sca-1 shRNA (D8) and probed by Western blotting for expression of Sca-1, pSer84PPARγ, PPARγ, pERK1/2, ERK1/2, PTEN, and β-actin. Reduction of Sca-1 increased PPARγ and reduced the percentage of pSer84PPARγ and pERK. B, bar graphs of the Western blots shown in A. C, GW7845 increases PPARγ expression. 34T and D8 cells in A were treated overnight with 0.1 μmol/L GW7845. Bar graph indicates that GW7845 enhanced PPARγ levels to a greater extent in D8 cells than in 34T cells. D, effect of proteasome inhibition on pSer84PPARγ and PPARγ expression. 34T and D8 cells were treated overnight with 1 μmol/L lactacystin. Bar graph indicates that PPARγ expression is increased to a greater extent in 34T cells than in D8 cells. E, reduction of Sca-1 increases PTEN and FABP3 mRNA expression. 34T and D8 cells were analyzed for PTEN and FABP3 mRNA levels by qRT-PCR and all values were normalized to actin. There was a significant difference between 34T and D8 cells in PTEN mRNA levels (P < 0.01, N = 3) and FABP3 mRNA levels (P < 0.001, N = 3) by the 2-sided Student t test. F, schematic of the regulation of PPARγ by Sca-1. Sca-1 is envisioned to suppress PTEN in part through ERK-mediated inhibition of PPARγ. Phosphatidylinositol 3-kinase (PI3K)-dependent Ras/ERK signaling results in increased inhibition of PPARγ by ERK-mediated phosphorylation on Ser84, which in turn reduces PTEN transcription. The opposite effect occurs during Sca-1 deficiency, which results in reduced progenitor cell expansion, delayed tumorigenesis and increased sensitivity to PPARγ agonists. Hongyan Yuan et al. Cancer Prev Res 2012;5:51-60 ©2012 by American Association for Cancer Research