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NF-kB in cellular senescence

Wednesday, September 24, 2014 — Poster Session IV

10:00 a.m. –12:00 p.m.

FAES Academic Center




  • Jaimy Joy
  • Ranja Sen


Cellular senescence is a phenomenon characterized by an irreversible growth arrest attributable to telomeric attrition, oncogenic stimuli, or DNA damage. Senescent cells are known to secrete pro-inflammatory cytokines, termed the senescence associated secretory phenotype (SASP), which promotes age-related diseases. An important component of the senescent phenotype, including SASP, is NF-kB, a ubiquitous transcription factor critical in numerous cell processes. It has been previously demonstrated that NF-kB activity is increased in senescent cells and that knockdown of NF-kB subunits result in a reduction of SASP factors. Senescence in human diploid fibroblasts can be induced by treatment with etoposide and display the hallmark features of senescence, including the lack of proliferation by EdU incorporation, positive beta-galactosidase staining, increased p16INK4a expression, and the presence of heterochromatin foci. We seek to determine whether NF-kB is necessary for the initiation and maintenance of senescence. To do this, we will generate an inducible stable cell line that expresses dominant negative inhibitor of NF-kB alpha (IkBa), which allows control of canonical NF-kB signaling. This system will allow us to determine whether the senescent phenotype can be reversed in the absence of NF-kB signaling and if overexpression of canonical NF-kB signaling can drive a cell into senescence.

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