Inflammation-driven cancer: role of ERK5 on Tumour-associated macrophages

Il 31/05/2019 ore 14.30 - 15.30

Sala conferenze Cnr, Area della ricerca Na1, via Pietro Castellino 111, 80131 Napoli

Emanuele Giurisato (from the Department of Biotechnology Chemistry & Pharmacy - Department of Excellence 2018-2022 - University of Siena, Italy) will give a seminar on 'Inflammation-driven cancer: role of ERK5 on Tumour-associated macrophages'.

The inflammatory microenvironment is arguably one of the most influential components of most, if not all, tumours. Central to cancer-related inflammation is a population of macrophages, namely tumour-associated macrophages (TAMs), and their presence often correlates with reduced survival in most cancers. Notably, TAMs can enhance malignancy and tumour resistance to treatment through stimulating angiogenesis, re-modeling the tumour extracellular matrix to aid invasion, and suppressing anti-tumour T cell immunity.

ERK5 belongs to the evolutionary conserved family of mitogen-activated protein kinases (MAPKs). However, ERK5 is different from the other MAPKs due to a unique extended C-terminal tail that contains a transcriptional activation domain and a nuclear localisation sequence. These features clearly indicate unique mechanisms of downstream regulation of targets. The importance of ERK5 in signal transduction is further supported by genetic evidence that the pathway exerts non-redundant functions in vivo. More recently, it has been shown that suppressing inflammation by inducing erk5 deletion in neoplastic keratinocytes reduced tumour burden. Moreover, we have discovered that targeted ablation of ERK5 in macrophages halted the growth of carcinoma and melanoma grafts. This tumour growth defect correlated with reduced tumour vasculature and macrophage density, in addition to abnormal macrophage polarisation.


Organizzato da:

Referente organizzativo:
Diana Boraschi
Cnr - Istituto di biochimica delle proteine
Via Pietro Castellino 111, 80131 Napoli

Modalità di accesso: ingresso libero

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