Research Paper Volume 12, Issue 3 pp 2373—2392

UBE2M promotes cell proliferation via the β-catenin/cyclin D1 signaling in hepatocellular carcinoma


Figure 6. UBE2M mediates tumor growth in a xenograft HCC model. (A) Images of the tumors that develop in nude mice treated with UBE2M-knockdown MHCC-97L cells or control cells (upper panel), as well as UBE2M-overexpression BEL-7402 cells or control cells (lower panel). (B) Tumor volume was measured at the indicated time points, and the tumor growth curve was shown using a time-course line plot in the indicated group (n=5 per group). (C) Tumor weight was recorded on the 27th day after the mice were sacrificed in the indicated group (n=5 per group). (D) The expression of UBE2M, cyclin D1, c-Myc, and β-catenin in the tumors of indicated group by Western blotting. (E) Representative Hematoxylin and eosin (HE) and immunohistochemical staining of HCC tumors for UBE2M, cyclin D1, β-catenin, anti-PCNA and Ki67 expression. (×100: Scale bar, 50 μm. ×400: Scale bar, 12.5 μm). (F) Schematic of working model. Upregulated UBE2M translocates accumulated β-catenin from the cytoplasm to the nucleus, thus activating downstream β-catenin/cyclin D1 signaling to promote cell cycle and proliferation. Data were expressed as mean ± SD (n = 5). *P < 0.05; **P < 0.01; ***P < 0.001 (student’s t-test).