RT Journal Article
SR Electronic
T1 DDX5 promotes oncogene C3 and FABP1 expressions and drives intestinal inflammation and tumorigenesis
JF Life Science Alliance
JO Life Sci. Alliance
FD Life Science Alliance LLC
SP e202000772
DO 10.26508/lsa.202000772
VO 3
IS 10
A1 Nazia Abbasi
A1 Tianyun Long
A1 Yuxin Li
A1 Brian A Yee
A1 Benjamin S Cho
A1 Juan E Hernandez
A1 Evelyn Ma
A1 Parth R Patel
A1 Debashis Sahoo
A1 Ibrahim M Sayed
A1 Nissi Varki
A1 Soumita Das
A1 Pradipta Ghosh
A1 Gene W Yeo
A1 Wendy Jia Men Huang
YR 2020
UL https://www.life-science-alliance.org/content/3/10/e202000772.abstract
AB Tumorigenesis in different segments of the intestinal tract involves tissue-specific oncogenic drivers. In the colon, complement component 3 (C3) activation is a major contributor to inflammation and malignancies. By contrast, tumorigenesis in the small intestine involves fatty acid–binding protein 1 (FABP1). However, little is known of the upstream mechanisms driving their expressions in different segments of the intestinal tract. Here, we report that the RNA-binding protein DDX5 binds to the mRNA transcripts of C3 and Fabp1 to augment their expressions posttranscriptionally. Knocking out DDX5 in epithelial cells protected mice from intestinal tumorigenesis and dextran sodium sulfate (DSS)–induced colitis. Identification of DDX5 as a common upstream regulator of tissue-specific oncogenic molecules provides an excellent therapeutic target for intestinal diseases.