Model of SWI/SNF, Keap1, and C9orf82 regulating different phases of Topo II poison-induced DNA break formation and DDR. Topo II poisons like doxorubicin.

Slides:



Advertisements
Similar presentations
Cancer Accelerated Biology. Learning Objectives The different methods of diagnosing cancer. The difference between a malignant tumor and a benign tumor.
Advertisements

Cell Cycle Regulation. The Cell Cycle What can be learned from this experiment? There are different signals (proteins) present that aid in the progression.
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,
Enhanced DNA damage in IDH1 mutant glioma cells.
Targeting the DNA Damage Response in Cancer
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
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 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.
miR-133a positively regulated p53/p21 pathway.
Oh what a tangled web it weaves: BRCA1 and DNA decatenation
Biological targets and phase II metabolism of chemopreventive licorice compounds. Biological targets and phase II metabolism of chemopreventive licorice.
Do DNA Double-Strand Breaks Drive Aging?
Figure 1 Chronic inflammation and DNA damage in people with SLE
Figure 3 Nuclear-penetrating autoantibodies and synthetic lethality
TDP1 knockdown increases the sensitivity of rhabdomyosarcoma cell lines to CPT treatment. TDP1 knockdown increases the sensitivity of rhabdomyosarcoma.
Proposed model of the tumor-suppressive effects of TPL2 in the lung.
Hypothetical model of HvAP2 control of stem elongation.
Model for the regulation of HIPK2 activity and p53 phosphorylations by the ATM pathway. Model for the regulation of HIPK2 activity and p53 phosphorylations.
Loss of Drp1 induces replication stress-mediated genome instability.
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.
Representative Western blot analyses of S-phase and other proteins from PC3 cell lysates obtained 3 days after oligomer (400 nm)/Lipofectin (15 μg/ml)
Induction of CDKN1A (□), MDM2 (◊), and GADD45A (○) in ML-1 cells by 50 cGy X-rays delivered at 0.28 cGy/min. Induction of CDKN1A (□), MDM2 (◊), and GADD45A.
Synergistic effect of CNP and doxorubicin (DOX) on thiol oxidation.
C-MYC controls expression of ABC drug transporters in CD34+ hematopoietic progenitors. c-MYC controls expression of ABC drug transporters in CD34+ hematopoietic.
Evaluation of top candidate clones for selective killing in bispecific antibody format. Evaluation of top candidate clones for selective killing in bispecific.
Protein expression profile in a dasatinib-resistant cell line.
PELP1 regulates the expression and activities of MMPs in ER-negative cells. PELP1 regulates the expression and activities of MMPs in ER-negative cells.
CNDT2.5 cells express mRNA for synaptophysin and neuron-specific enolase. CNDT2.5 cells express mRNA for synaptophysin and neuron-specific enolase. RT-PCR.
Quercetin induces arrest in G1 phase of cell cycle in P39 xenografts.
Ki-67 expression is dynamically controlled by a cell-cycle–regulatory network. Ki-67 expression is dynamically controlled by a cell-cycle–regulatory network.
A, top, representative Western blot for Ku70 in MCF7 cell extracts following siRNA knockdown of Ku70, compared with siRNA control. A, top, representative.
Knockdown of PKM2 suppressed TPA-induced skin cell transformation.
High-throughput siRNA screening results and corresponding patient gene expression data for PP2A subunits. High-throughput siRNA screening results and corresponding.
Specific up-regulation and down-regulation of immunomodulatory genes in human breast and colorectal cancers. Specific up-regulation and down-regulation.
A, Proportion of variants detected in the MMR genes.
Alkaline Comet assay showing DNA break formation after 6-TG treatment, implying more SSBs generated in MMR+ cells. Alkaline Comet assay showing DNA break.
Effect of bFGF on ultrastructure of RD-ES cells.
Effect of coapplication of dexrazoxane and doxorubicin on DSB formation, TOP2A protein level, and apoptosis. Effect of coapplication of dexrazoxane and.
Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. LNCaP,
A, P causes G2-M arrest with apoptosis in asynchronous population of PC-3 when exposed to 1.5 and 5 μmol/L P for various time points. A, P
Induction of DNA strand breaks by artesunate.
Induction of apoptosis in mismatch repair-deficient tumor cell lines after microinjection of phMSH2 and phMLH1 cDNA expression constructs. Induction of.
Potential model of HMQ1611 inhibiting breast cancer cell proliferation
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.
Bortezomib induces an NRF2 signature and NRF2 protein in tumor cells from leukemic MCL. Gene sets regulated by bortezomib (Supplementary Tables S3 and.
WP1066 inhibits the progression of OCIM2 cells through the cell cycle.
Characterization of DNA-PK and PARP-1 levels and activities in the cell lines studied. Characterization of DNA-PK and PARP-1 levels and activities in the.
Representative images demonstrating LOH in breast cancer patients’ paired BM aspirate and primary tumors (T) at D14S62, D14S51, and D8S321, respectively.
6-TG dose and time relationships for DSB formation using PFGE, demonstrating that the formation of DSBs in both MMR+ M4 and MMR− V2 cells is dose dependent.
DNA-binding and double-strand break formation by Vpr.
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.
p53 loss affects several steps of the metastatic process.
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.
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.
P53-expressing tumor cells circumvent mitosis, express markers consistent with a G1-like state, and become senescent in response to continuous chemotherapeutic.
BEZ235 induces accelerated senescence after radiation (IR) in vitro.
Establishment of HeLa/rtTAA/TRE-N1-IC cell line.
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.
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.
TNFα-expanded MRD cells acquire the recurrence-competent phenotype.
CPGL is a growth suppressor in pancreatic cancer cell lines.
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.
Investigation of reactivity of D14 HLA-A
Recruitment of CD8+, CD4+, and Foxp3+ cells into oral lesions in response to anti–PD-1 treatment. Recruitment of CD8+, CD4+, and Foxp3+ cells into oral.
Tobacco-specific carcinogens induce methylation, DNA adducts, DNA damage, and activation of DNMT1. Tobacco-specific carcinogens induce methylation, DNA.
Loss of NQO1 expression inhibits invasion of NSCLC
Presentation transcript:

Model of SWI/SNF, Keap1, and C9orf82 regulating different phases of Topo II poison-induced DNA break formation and DDR. Topo II poisons like doxorubicin induce DNA DSBs by trapping Topo II on the DNA. If not sufficiently repaired, this leads to cell death. Model of SWI/SNF, Keap1, and C9orf82 regulating different phases of Topo II poison-induced DNA break formation and DDR. Topo II poisons like doxorubicin induce DNA DSBs by trapping Topo II on the DNA. If not sufficiently repaired, this leads to cell death. Keap1 controls the expression of Topo IIα, while SWI/SNF regulates the loading and hereby activity of Topo IIα. Loss of these genes therefore attenuates DNA DSB formation by Topo II poisons. In the next phase of the DNA breaks and repair cycle, C9orf82 controls DNA repair. Loss of C9orf82 accelerates DNA repair, reducing cell death induced by Topo II poisons. Ruud H. Wijdeven et al. Cancer Res 2015;75:4176-4187 ©2015 by American Association for Cancer Research