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Status |
Public on Jun 06, 2021 |
Title |
ARID1A deficiency promotes pancreatic tumorigenesis by reducing KRAS-induced senescence (ATAC-Seq) |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
ARID1A is one of the most frequently mutated epigenetic regulators in a wide spectrum of cancers. In this study, we identified the anti-senescence effect of ARID1A deficiency in the progression of pancreatic intraepithelial neoplasia (PanIN) by profiling the transcriptome of individual PanINs in the mouse model. Interestingly, we found that ARID1A deficiency activates the transcription of Aldehyde dehydrogenase 1 family, member A1 (ALDH1A1), which play essential roles in attenuating the senescence by significantly reducing reactive oxygen species (ROS) induced by oncogenic KRAS. Our findings further suggest that ALDH could be considered as a potential adjuvant target for prevention and treatment of pancreatic cancer.
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Overall design |
We performed ATAC-seq on wild type HPNE cell line and ARID1A-KO HPNE cell line. Three biological replicates per group.
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Contributor(s) |
Zong C, Liu S, Cao W, Niu Y |
Citation(s) |
33983114 |
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Submission date |
Oct 29, 2020 |
Last update date |
Sep 05, 2021 |
Contact name |
Chenghang Zong |
E-mail(s) |
chenghang.zong@bcm.edu
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Organization name |
Baylor College of Medicine
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Lab |
Zong Lab
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Street address |
1 Baylor Plaza
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City |
Houston |
State/province |
TX |
ZIP/Postal code |
77030 |
Country |
USA |
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Platforms (1) |
GPL18573 |
Illumina NextSeq 500 (Homo sapiens) |
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Samples (6)
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This SubSeries is part of SuperSeries: |
GSE160444 |
ARID1A deficiency promotes pancreatic tumorigenesis by reducing KRAS-induced senescence |
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Relations |
BioProject |
PRJNA673201 |
SRA |
SRP289788 |