Effects of low-level expression of mutant-template telomerase RNA in MCF-7 breast cancer cells. Effects of low-level expression of mutant-template telomerase.

Slides:



Advertisements
Similar presentations
8 miles © All material in this document is protected by copyright, and must not be reproduced without the express permission of the Motorway Archive Trust.
Advertisements

Control of Gene Expression
Cancer. Cancer is a disease of the cell cycle Caused by one or more of the following: Increase in growth signals Loss of inhibitory signals In addition,
An antiapoptotic role for telomerase RNA in human immune cells independent of telomere integrity or telomerase enzymatic activity by Francesca S. Gazzaniga,
Telomerase Activity and Expression of Telomerase RNA Component and Telomerase Catalytic Subunit Gene in Cervical Cancer Kenji Nakano, Elizabeth Watney,
Perturbations in desmin filament network formation in cells expressing a recombinant desmin protein harboring a 7-amino-acid deletion found in a patient.
Enhanced DNA damage in IDH1 mutant glioma cells.
Targeting the PARP DNA repair pathway enhanced cytotoxicity induced by chemotherapy. Targeting the PARP DNA repair pathway enhanced cytotoxicity induced.
IDH1 mutant glioma cells are sensitive to TMZ
سرطان الثدي Breast Cancer
Figure 3 Intracranial targeting of high-grade gliomas
Plots derived from provisional TCGA data from sequencing and expression analyses of invasive breast carcinoma cases. Plots derived from provisional TCGA.
Vemuri B. Reddy, PhD, Thomas A
Pancreatic Cancer: Basic and Clinical Aspects
J Bone Miner Res 2015;30:1553 (Fig. 1)
The 3D models in part a are reproduced with permission from Daum, B
Cetuximab treatment increases IFNγ receptor 1 expression.
ATF5 transactivates Egr-1 via the ATF5CON sites in the Egr-1 promoter.
Figure 2 Luciferase assays of transiently transfected HEK 293 cells with reporter constructs containing the 766-bp wild-type KCNJ18 or c.-542 T/A mutant.
Vemuri B. Reddy, PhD, Thomas A
Bone 2013;56:23 (Fig. 1) Reproduced from Bone, 56:23-9, Copyright (2013), with permission from Elsevier.
Strategy for mutant telomere synthesis in human cancer cells.
Knockdown of endogenous WT-hTER by a short hairpin RNA (siRNA) directed specifically against the human WT telomerase RNA template. Knockdown of endogenous.
DNA damage foci accumulate at a subset of telomeres in cells expressing a mutant-template telomerase RNA. Immunostaining was done for telomere-protective.
CYP1A1 knockdown increases cell death.
Bone 2014;69C:89 (Fig. 2) Reproduced from Bone, 69C:89-97, Copyright (2014), with permission from Elsevier.
A, B, apoptosis analysis using Annexin V-FITC/PI was done on 5th, 7th, and 9th day after transfection either with si control or si AEBP1in U87MG and U138MG.
J Bone Miner Res 2014;doi: /jbmr.2325 (Fig. 2)
Figure 4. MicroRNA (miR)-195 and miR-497 directly targets CD274
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.
A, chemical structures of PRIMA-1 and PRIMA-1Met.
Representative examples of estrogen receptor α and β immunohistochemical expression (top figures) and EGFR mutations (bottom figures) in lung adenocarcinomas.
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.
Clathrin-dependent, constitutive endocytosis of DR4 and DR5 in TRAIL-resistant cells. Clathrin-dependent, constitutive endocytosis of DR4 and DR5 in TRAIL-resistant.
Greater induction of apoptosis following EGFR TKI treatment correlates with higher basal BIM expression across a panel of EGFR-mutant lung cancers. Greater.
Expression of CRC stem cell markers and L1 in CRC cells.
EN1-associated chromatin complexes in breast cancer cells.
A, RT-PCR expression of matriptase-1 and matriptase-2 in a variety of 24 human cell lines. A, RT-PCR expression of matriptase-1 and matriptase-2 in a variety.
SAF-1 expression in clinical breast cancer tissues.
Effect of IL24 on phosphorylation of eIF2α and proliferation in cancer cells. Effect of IL24 on phosphorylation of eIF2α and proliferation in cancer cells.
Induction of apoptosis in human embryonic kidney 293 cells injected with phMSH2 or phMLH1 cDNA expression constructs. Induction of apoptosis in human embryonic.
Northern blot analysis of maspin in cancer cell lines and human tissues. Northern blot analysis of maspin in cancer cell lines and human tissues. A, HMECs.
Effect of hydrogen peroxide on survival and transcriptional activation of TFF1 in established cell lines from the following human tumor tissues: breast.
Activation of membrane-associated Akt is associated with loss of apoptosis in TgAPT121;Pten+/− prostates. Activation of membrane-associated Akt is associated.
Kaplan-Meier survival analysis of p53 mutation in the overall breast tumor series. Kaplan-Meier survival analysis of p53 mutation in the overall breast.
A and B, comparison of time course of TFF1 mRNA induction under estrogen-withdrawn (denoted ph−/ES−) and estrogenic medium (denoted ph+/ES+) conditions.
Pirh2 represses p73-dependent transactivation.
Nested RT-PCR of Mammaglobin and CK19 mRNA in plasma and circulating cells of controls (C) and patients (T) with breast cancer. Nested RT-PCR of Mammaglobin.
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.
PTPH1 depends on its catalytic activity to increase ER nuclear accumulation and to enhance breast cancer sensitivity to TAM. A, effects of PTPH1 and PTPH1/DA.
Establishment of MajSAT RNA–expressing mice.
PD-L1 is expressed in breast cancer.
Expression of versican promoted breast cancer cell tumor formation and self-renewal in vivo. Expression of versican promoted breast cancer cell tumor formation.
Met is expressed in Her2-overexpressing cell lines and Her2 (+) breast tumors. Met is expressed in Her2-overexpressing cell lines and Her2 (+) breast tumors.
The Ser124 site of Cdc25A is required for Cdc25A degradation in response to I3C induction. The Ser124 site of Cdc25A is required for Cdc25A degradation.
Delineating cancer evolution with single-cell sequencing
Transcriptional activity and growth of mutant ER in a breast cancer cell line. Transcriptional activity and growth of mutant ER in a breast cancer cell.
VEGF165 stimulates migration of HMVECs
AR inhibition decreases ER+/AR+ breast cancer growth.
Comparison of Akt1 and Akt3 for their abilities to activate the Fra-1 promoter. Comparison of Akt1 and Akt3 for their abilities to activate the Fra-1 promoter.
The activation of PKC-δ and JNK1 is essential for doxorubicin-induced senescence. The activation of PKC-δ and JNK1 is essential for doxorubicin-induced.
Expression data from genes involved in regulation of transit through the cell cycle in response to treatment with E2 and OHT. A. Expression data from genes.
Establishment of HeLa/rtTAA/TRE-N1-IC cell line.
In the presence of human monocytes, estradiol increased breast cancer cell dissemination to the periphery via CCL2 and CCL5. In the presence of human monocytes,
RRP1B interacts with TRIM28 and HP1α at regions associated with H3K9me3 and decreased gene expression. RRP1B interacts with TRIM28 and HP1α at regions.
Expression of chemokine receptors in A-498 cell line.
Investigation of reactivity of D14 HLA-A
I3C reduces the level of Cdc25A protein in breast cancer cells.
miR-181a knockdown inhibits VEGF and MMP1 secretion in vitro.
An NH2-terminal domain of PALB2, distinct from the BRCA2-interacting domain of PALB2, mediates interaction with BRCA1 and assembly of PALB2 nuclear foci.
Presentation transcript:

Effects of low-level expression of mutant-template telomerase RNA in MCF-7 breast cancer cells. Effects of low-level expression of mutant-template telomerase RNA in MCF-7 breast cancer cells. Apoptosis was quantified in clonal lines stably expressing low levels of a mutant-template telomerase RNA construct, a control wild-type RNA construct, or parental MCF-7 cells. Reproduced from the Proceedings of the National Academy of Sciences, U.S.A., 2001;98:7982–7 by copyright permission of the National Academy of Sciences, U.S.A. (5). Elizabeth H. Blackburn Mol Cancer Res 2005;3:477-482 ©2005 by American Association for Cancer Research