Blocking NFATc3 ameliorates azoxymethane/dextran sulfate sodium induced colitis-associated colorectal cancer in mice via the inhibition of inflammatory responses and epithelial-mesenchymal transition.

In conclusion, NFATc3 was involved in the pathogenesis of experimental UC-CRC and NFATc3 knockdown ameliorated experimental UC-CRC progression via the inhibition of inflammatory responses and EMT. NFATc3 mediated the inhibitory effects of miR-370-3p on CRC cells proliferation and EMT. Targeting NFATc3 may be effective in treating UC-CRC. PMID: 32653643 [PubMed - as supplied by publisher]

https://www.ncbi.nlm.nih.gov/pubmed/32653643?dopt=Abstract

Source: Cellular Signalling - July 8, 2020 Category: Cytology Authors: Lin Y, Koumba MH, Qu S, Wang D, Lin L Tags: Cell Signal Source Type: research