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The Senescence-Associated Innate Immune Sensors in Tumour Suppression

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  • UserDr Juan Carlos Acosta; Cancer Research UK Edinburgh Centre, MRC Institute of Genetics & Molecular Medicine
  • ClockFriday 03 July 2020, 15:00-16:00
  • HouseZoom Seminar.

If you have a question about this talk, please contact Bobbie Claxton.

This seminar will be online via zoom

Cellular senescence is a tumour suppressor response that impairs the propagation of mutated cells, characterized by a robust cell cycle arrest and the senescence-associated secretory phenotype (SASP), a pro-inflammatory secretome that reinforces senescence and promotes immune-clearance of senescent cells. Cellular senescence is the outcome of most conventional and pro-senescence anti-cancer treatments. However, accumulation of cancer-associated senescent cells during tumour initiation, ageing, or cancer treatments can facilitate cancer progression through the paracrine effects of the SASP or by senescent cell reprogramming to a cancer stem cell-like state. Therefore, novel strategies for controlling the adverse effects of cancer-associated senescent cells by SASP manipulation or by senescent cell elimination (senolytics) are urgently needed. Previously, we discovered that the SASP depends on the activation of the inflammasome, a molecular platform for Caspase-1 (CASP1) induction downstream of innate immune receptors. Inflammasomes are assembled by the activation of Pattern Recognition Receptors (PRRs). PRRs are sensors of the innate immune system which recognize Pathogen Associated Molecular Patterns (PAMPs) abundant in pathogens but absent in the host (i.g. LPS of Gram-negative bacteria), and endogenous molecules from the host activated upon stress and damage or Damage Associated Molecular Patterns (DAMPs) (i.e. HMGB1 or alarmin). During the seminar, I will show our recent work identifying the essential role for the senescence-associated innate immune sensor Toll-Like Receptor 2 (TLR2) regulating the SASP in oncogene-induced senescence (OIS), and the identification of the serum amyloids SAA1 /2 as the specific DAMP for TLR2 . Moreover, I will show our efforts to demonstrate a tumour suppressor role of TLR2 in non-small cell lung carcinoma. Finally, I will introduce our last results uncovering the new and specific mechanism of inflammasome activation in OIS and discuss our efforts to exploit the inflammasome for new treatments in cancer by stimulation the inflammatory cell death pyroptosis in cancer cells.

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