top of page

The Ronai Lab studies signaling networks that are deregulated in cancer in order to understand how to correct them. We focus on pathways that are engaged in the control of RNA translation, splicing and protein homeostasis, both in tumors per se as in their microenvironment, realizing that the cross talk between the tumors and their environment dictates their fate – ability to grow, resist therapy as well as metastasize.

Traditionally, the lab studied epigenetic regulators in tumors, from ubiquitin ligases (RNF5 and Siah1a/2) to PRMT5 or GCDH. The common driver in a number of our studies was found to be the UPR with ATF4 standing out. How diverse signaling pathways can impact ATF4 activities to elicit its pro-apoptotic or pro-survival signaling is an ongoing research interest. Further, the relationship between activities in immune cells, in stroma and those that are tumor intrinsic, underlie much of our ongoing studies. 

Our studies are guided by data from relevant cancer patient specimens, coupled with advanced bioinformatics, which allow us to predict pathways that are then tested in genetic models and relevant 2D and 3D cultures. When applicable, we advance our mechanistic understanding with the development of small molecule inhibitors that may offer novel therapeutic modalities. Among those are our studies with inhibitors of the translational initiation complex, and with small molecule inhibitors of GCDH, to which melanoma are addicted to.

bottom of page