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Data · dataset · 2014

Gene expression profiling of replicative and induced senescence

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Cellular senescence is a cell cycle arrest accompanied by high expression of cyclin dependent kinase inhibitors which counteract overactive growth signals, which serves as a tumor suppressive mechanism.

Description

Senescence can be a result of telomere shortening (natural or replicative senescence) or DNA damage resulting from exogenous stressors (induced senescence). Here, we performed gene expression profiling through RNA-seq of replicative senescence, adriamycin-induced senescence, H 2 O 2 -induced senescence, and 5-aza-2-deoxycytidine-induced senescence in order to profile the pathways controlling various types of senescence.

Overall, the pathways common to all 4 types of senescence were related to inflammation and the innate immune system. It was also evident that 5-aza-induced senescence mirrors natural replicative senescence due to telomere shortening. We also examined the prevalence of senescence-associated secretory phenotype (SASP) factors in the RNA-seq data, showing that it is a common characteristic of all 4 types of senescence.

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In addition, we could discriminate changes in gene expression due to quiescence during cellular senescence from those that were specific to senescence.

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Cancer
Inferred from text
RNA sequencing 65%

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Provenance · 1 source records, 12 field assertions
SourceKeyLast seenRaw
DataCite10.6084/m9.figshare.128440013 d agoJSON v1
FieldAssertionExtractorEvidence
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concepts[disease].local:disease:cancermapping · DataCitevocabulary-mapper@1.0.0keywords['Cancer']
concepts[field].fos:biological-sciencessource · DataCiteconnector:datacite@1.0.0
concepts[field].fos:clinical-medicinesource · DataCiteconnector:datacite@1.0.0
concepts[modality].local:modality:rna-seqenrichment · DataCitekeyword-concept-rules@1.0.0title+description (65%)
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