Cellular senescence in development, regeneration and cancer
Dr Manuel COLLADO
Health Research Institute of Santiago de Compostela (IDIS), Spain
Tuesday, November 26th 2019 - 3:30 p.m.
- Auditorium, IGBMC
Hosted by Bill KEYES
Cellular senescence is a state of permanent cell cycle arrest undergone by normal primary cells when they exhaust their replicative potential. Although it was originally described as the basis of aging, it is now clear that different situations causing cellular stress can trigger senescence as a defense mechanism to avoid the unrestricted proliferation of damaged cells. This function of senescence represents a crucial tumor suppressor mechanism that cancer cells need to bypass to grow and form tumors. Despite that, cancer cells can still be induced into senescence by triggering the right signaling pathways in the cell, something that some chemotherapeutic drugs can actually do. However, senescent tumor cells represent a potential risk for the patients since these “zombie” cancer cells could escape the control of senescence to regrow as more malignant and aggressive tumors. To improve a potential prosenescence therapy of cancer we need to identify compounds with specific cytotoxic activity directed against senescent cells, the so-called senolytic compounds. We have identified a family of compounds with this senolytic activity that we will present in our talk.
In recent years, we have also undercover novel physiological functions of cellular senescence as a remodeling and morphogenetic force during embryo development, and as a process involved in tissue repair and regeneration. I will present some of the new data we have obtained in this sense.