Skip to main content
. Author manuscript; available in PMC: 2020 Feb 15.
Published in final edited form as: Cancer Res. 2018 Nov 12;79(4):706–719. doi: 10.1158/0008-5472.CAN-18-1207

Figure 5.

Figure 5.

miR-23a-3p mediates the effects of MasR activation of myosin-4. (A). MHCIIa, MHCIIx and MHCIIb mRNA expression in C2C12 myotubes co-cultured for 48 h with or without C-26 cancer cells (unpaired t test; *P<0.02; n=6). (B) Ingenuity Pathway Analysis (IPA) revealed microRNA-23a (miR-23a-3p) as a mediator of MasR regulation of Myh4. The binding site on the 3’UTR of Myh4 mRNA for the seed sequence of miR-23a. (C, D) C2C12 myoblasts were transfected with a miRNA mimic negative control (-ve control) or miR-23a-3p mimic and after 4 days of differentiation into myotubes, were co-cultured with C-26 cancer cells and treated with vehicle or AVE0991 and assessed 48 h later for myotube diameter. Overexpression of miR-23a-3p using a mimic attenuated the AVE0991 induced increase in size of myotubes co-cultured with C-26 cells (unpaired t test; **P<0.01; n=6).