Non-cell autonomous roles of telomere shortening in zebrafish

authors

• Mariana Gil
• Figueira Margarida
• Ferreira Miguel G.
• Gil Mariana M
• Maouche Ahmed
• Serifoglu Naz
• Figueira Margarida
• Ferreira Miguel Godinho

keywords

• And MGF performed research
• KG
• MM
• KL
• And MGF designed research
• MF
• BL-B
• MMG
• Author contributions KL
• And MF contributed new reagents/analytic tools
• TC
• And MGF analyzed data
• MGF acquired funding and coordinated the work
• And KL
• And MGF wrote the paper

abstract

Background: Cancer incidence increases with age. Due to the end-replicative problem, telomeres shorten with each cell division throughout our lives. Telomere shortening has consequences beyond the cellular level. As we age, cells approach replicative senescence and DNA damage emanating by short telomeres initiate a cascade of events that expands to the extracellular environment. Senescent cells were shown to release a set of molecules including inflammatory cytokines, termed senescence-associated secretory phenotype (SASP). Indeed, an inflammatory environment generates a pro-tumorigenic environment that supports tumor invasiveness. Aim of the study: Investigate the causal relation between short telomeres and cancer incidence. Determine whether this effect has a non-cell autonomous component by using zebrafish embryo chimeras and tumor transplants.

more information