Journal
CELL CYCLE
Volume 13, Issue 24, Pages 3927-3937Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/15384101.2014.973327
Keywords
adriamycin; aging; hydrogen peroxide; Li Fraumeni Syndrome; RNA-seq; Senescence; 5-aza-2'-deoxycytidine; H2O2; hydrogen peroxide; 5-aza; 5-aza-2-deoxycytidine; LFS; Li-Fraumeni Syndrome; adria; adriamycin; nat; natural; LLP; lowest passage; LP; low passage; IFN; interferon; IPA; Ingenuity Pathway Analysis; GGA; Genomatix Genome Analyzer; SPIA; Signaling Pathway Impact Analysis
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Funding
- Barbara and Fred Erb Endowed Chair in Cancer Genetics
- Karmanos Cancer Institute
- Molecular Medicine and Genetics Applied Genomics Technology Center at Wayne State University and the Karmanos Cancer Institute [P30CA022453]
- DeRoy Testamentary Foundation Fellowship
- Graduate Research Assistant Fellowship from Wayne State University
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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. 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, H2O2-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. 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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