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BRD4 inhibitor JQ1 increase the sensitivity of arsenic trioxide in pancreatic cancer

ABSTRACT: BRD4 inhibitor JQ1 increase the sensitivity of arsenic trioxide in pancreatic cancer

PROVIDER: PRJNA510651 | ENA |

REPOSITORIES: ENA

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BRD4 inhibitor JQ1 increase the sensitivity of arsenic trioxide in pancreatic cancer

Project description:Pancreatic cancer is a deadliest type of malignancy, largely due to lack of effective intervention. We here report a pair of agents, ATO and JQ1, which synergistically induce apoptosis in the malignancy. Through global and molecular approaches, we have provided evidence that these agents are both able to modulate ER stress and autophagy in the cancer, probably acting in different ways. Cross-talks between ER stress and autophagy are implicated during ATO/ATO plus JQ1 induced apoptosis, in which NRF2 appears to play a central role. of the globe transcriptional profiles of ATO regulated genes in breast, colon and lung cancer cells with different p53 status. We find p53 wild type cells are resistant to ATO induced globe dynamic transcriptional changes, thus resistant to ATO induced cell growth inhibition. P53 inhibitor PFTα releases p53 mediated transcriptional resistance and increases the sensitivity of ATO in p53 wild type tumor cells.

2019-12-31 | GSE124069 | GEO

Aberrantly expressed genes in HaCaT keratinocytes chronically exposed to arsenic trioxide

2012-04-12 | GSE37192 | GEO

Aberrantly expressed genes in HaCaT keratinocytes chronically exposed to arsenic trioxide

Project description:The purpose of this study is to search for aberrant genes in HaCaT keratinocytes after chronic exposure to arsenic trioxide. The objective of the investigation was to discover the mechanism of arsenic carcinogenicity in human epidermal keratinocytes. We hypothesize that a combined strategy of DNA microarray, qRT-PCR and gene function annotation will identify aberrantly expressed genes in HaCaT keratinocyte cell line after chronic treatment with arsenic trioxide. HaCaT cells were chronically exposed to 0.5M-BM-5g/mL arsenic trioxide (As2O3) up to 22 passages and RNA was extracted. Microarray data analysis identified 14 up-regulated genes and 21 down-regulated genes in response to arsenic trioxide Two experimental groups: 1. The treatment group was sub-cultured up to passage 22 to establish a chronic exposure state. 2. The passage control group was also sub-cultured up to 22 passages but with no exposure to arsenic trioxide. 4 technical replicates with 3 replicates making a total of 8X3 =24 samples HaCat Cell untreated (passage control): 1. H1_H001, H1_H002, H1_H003 2. H2_ H004, H2_H005, H2_H006 3. H3_ H007, H3_H008, H3_H009 4. H4_ H010, H4_H011, H4_H012 HaCat Cell treated with 0.5M-BM-5g/ml of arsenic trioxide: 5. A1_H013, A1_H014, A1_H015 6. A2_H016, A2_H017, A2_H018 7. A3_H019, A3_H020, A3_H021 8. A4_H022, A4_H023, A4_H024 Cell Type: Human Skin Keratinocyte: 1.5 M-CM-^W105 HaCaT cells were cultured in 7.5 ml of complete DMEM containing 10% Fetal Bovine Serum (FBS) and 1% penicillin, streptomycin in T-25 culture plate. Cells were incubated in a humidified atmosphere with 5% CO2 at 37 M-BM-:C. The treatment groups were exposed to 0.5M-BM-5g/mL As2O3 (equivalent to LC 0.5), and passaged at 90% confluent. Total RNA was extracted from 4 technical replicates of unexposed HaCaT cells and HaCaT cells chronically exposed to arsenic trioxide up to passage 22 using RNA STAT-60 (TEL-TEST, INC, Friendswood, TX, USA).

2012-04-11 | E-GEOD-37192 | biostudies-arrayexpress

Transcriptome analysis of mutant p53 rescued by arsenic trioxide (ATO)

Project description:The goals of this study are to compare transcriptome of mutant p53 rescued by arsenic trioxide

2022-12-12 | GSE141892 | GEO

Transcriptome analysis of mutant p53 (p53-V272M, p53-R282W) rescued by arsenic trioxide (ATO)

Project description:The goals of this study are to compare transcriptome of mutant p53 rescued by arsenic trioxide

2023-06-03 | GSE151696 | GEO

DNA microarray analysis for HepG2 cells exposed to arsenic trioxide

Project description:DNA microarray analysis revealed that the genes related to cell cycle regulation were significantly induced at non- and sub-lethal concentrations (i.e., 0.05-6 M-BM-5M), while the common feature of heavy metal toxicity such as oxidative damage and following increase in glutathione, heat shock proteins, and metallothionein were confirmed at high concentrations (i.e., 6-40 M-BM-5M). The concentration dependent modulation of gene expression (induction of cell cycle genes, induction of cell cycle arrest genes and apoptotic genes) following exposure to arsenic was further supported by acceleration of cell proliferation, ROS generation, and cytotoxicity. Furthermore, three cell cycle genes (i.e., CDC25B, UBE2C, and PTTG1) were proposed as marker genes of inorganic arsenic exposure. Those results indicated the potential pro-carcinogenic actions of inorganic arsenic occur in environmentally relevant exposures (as low as 0.07 M-BM-5M). In this study, we examined the gene expression alteration in HepG2 cells exposed to arsenic trioxide (5 nM to 40 M-BM-5M as As2O3 for 48 hours) by DNA microarray with 8795 human genes. HepG2 cells were also exposed to M-NM-5-caprolactam as a reference of non carcinogen since it is the only chemical categorized in IARCM-bM-^@M-^Ys group 4 (Probably Not Carcinogenic). MQ water was used as control. For replicate, three dishes were prepared for each sample and individually treated in parallel.

2013-07-02 | E-GEOD-48441 | biostudies-arrayexpress

The genomic landscape of sensitivity to Arsenic Trioxide characterized by Genome-wide CRISPR-Cas9 screening

Project description:The key modifiers of sensitivity to Arsenic Trioxide (ATO) remained unclear, and we presented a genome-wide scale loss-of-function screening to identify the modulators of cell response to ATO.

2023-04-24 | GSE218982 | GEO

Comparison of gene expression profile of naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

Project description:The aim of this study was to gain insight into the potential mechanism of resistance to arsenic trioxide (ATO). The gene expression profile of naive (NB4) (Acute promyelocytic leukemia (APL) cell line and one of its in house generated ATO resistant sub clone (NB4-VM-AsR1) was done using whole genome microarray and compared to generate the differential expression profile which will give insight into the mechanisms of ATO resistance in APL. Agilent one-color experiment,Organism: Human ,Agilent Whole Genome Human 4x44k (AMADID: 014850) , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442) naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

2013-08-02 | E-GEOD-42031 | biostudies-arrayexpress

Arsenic Trioxide, Fluorouracil, and Leucovorin in Treating Patients With Stage IV Colorectal Cancer That Has Relapsed or Not Responded to Treatment

Project description:RATIONALE: Drugs used in chemotherapy, such as fluorouracil and leucovorin, work in different ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing. Arsenic trioxide may help fluorouracil and leucovorin work better by making tumor cells more sensitive to the drugs. Giving arsenic trioxide together with fluorouracil and leucovorin may kill more tumor cells. PURPOSE: This phase I trial is studying the side effects and best dose of arsenic trioxide and fluorouracil when given together with leucovorin in treating patients with stage IV colorectal cancer that has relapsed or not responded to treatment.

| 2038167 | ecrin-mdr-crc

Clinical trial of intravenous arsenic trioxide in the treatment of advanced refractory colorectal cancer carrying structural mutant p53 gene

Project description:Interventions: Experimental group:intravenous arsenic trioxide Primary outcome(s): Objective response rate Study Design: Single arm

| 2692740 | ecrin-mdr-crc

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