EXPERIMENT_TITLE: GSM4977752: Hi-C_OFF_inverted; Homo sapiens; Hi-C
EXPERIMENT_DESIGN_LIBRARY_DESCRIPTOR_LIBRARY_CONSTRUCTION_PROTOC: In situ Hi-C on HBECs of different states and genotypes was performed and controlled for quality using the Arima Hi-C kit as per manufacturer's instructions. All resulting libraries that met the QC criteria set by the manufacturer were paired-end sequenced on a NovoSeq6000 platform (Illumina) to at least 0.5 billion reads. Standard Hi-C library construction on the basis of the Mate-pair kit (Illumina) 100-bp paired-end sequencing
STUDY_DESCRIPTOR_STUDY_ABSTRACT: Oncogene-induced senescence (OIS) is an inherent and important tumor suppressor mechanism. However, if not timely removed via immune surveillance, senescent cells will also present a detrimental side. Although this has mostly been attributed to the senescence-associated-secretory-phenotype (SASP) of these cells, we recently suggested that “escape” from the senescent state represents another unfavorable outcome. Here, we exploit genomic and functional data from a prototypical human epithelial cell model carrying an inducible CDC6 oncogene to identify an early-acquired recurrent chromosomal inversion, which harbors a locus encoding the circadian transcription factor BHLHE40. This inversion alone suffices for activation of BHLHE40 upon CDC6 induction and for driving cell cycle re-entry and malignant transformation. In summary, we provide strong evidence in support of genomic instability underlying “escape” from oncogene-induced senescence. Overall design: In situ Hi-C performed in two states (“OFF” and “Bypass”) of a single cell-derived HBEC clone carrying a CRISPR-generated >3-Mbp inversion on chr3 that encompasses the BHLHE40 gene locus
SAMPLE_TITLE: Hi-C_OFF_inverted
SAMPLE_SAMPLE_ATTRIBUTES_SAMPLE_ATTRIBUTE: [{"TAG": "source_name", "VALUE": "\u201cOFF\u201d HBECs"}, {"TAG": "cell type", "VALUE": "human bronchial epithelial cells"}, {"TAG": "sample type", "VALUE": "OFF"}]
Pool_Member_@attributes_sample_title: Hi-C_OFF_inverted
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