Research Paper Volume 12, Issue 18 pp 18192—18208

Figure 5. MiR-216a-3p enhances sorafenib sensitivity in the xenograft HCC tumor mouse model by attenuating MAPK14-dependent MEK-ERK and ATF2 signaling pathways. (A) Representative western blots show phospho-MEK1, MEK1, phospho-Erk1/2 and Erk1/2, phospho-ATF2 and ATF2 levels in sorafenib-treated Huh-7 cells transfected with shRNA-NC (negative control), shRNA-MAPK14, miR-NC (negative control), miR-216a-3p mimic respectively. (B) Comparison of saline or sorafenib treatment efficacy using Balb/c nude mice with xenograft tumors after injecting miR-NC, miR-216a-3p OE or miR-216a-3p KD Huh-7 cells. (C) The tumor size measurements and (D) tumor weight in saline or sorafenib-treated miR-NC, miR-216a-3p OE or miR-216a-3p KD groups of mice. (E) Western blot analysis show phospho-MAPK14, MAPK14, phospho-ATF2 and ATF2 levels in xenograft tumor tissues from saline or sorafenib-treated miR-NC, miR-216a-3p OE or miR-216a-3p KD groups of mice. (F) Representative IHC images show MAPK14 protein expression in xenograft tumor tissue sections from saline or sorafenib-treated miR-NC, miR-216a-3p OE or miR-216a-3p KD groups of mice. Also shown are H&E stained xenograft tumor tissue sections from saline or sorafenib-treated miR-NC, miR-216a-3p OE or miR-216a-3p KD groups of mice.