Skip to main content
. 2016 May 31;7(26):40266–40284. doi: 10.18632/oncotarget.9733

Figure 3. JARID2 significantly promotes invasion and metastasis of HCC cells in vitro and in vivo.

Figure 3

(A) Knockdown of JARID2 expression inhibited HCCLM3 (A1) and MHCC97-H (A2) cells migration, whereas overexpressed JARID2 in HepG2 cells promoted cell migration (A3) in wound-healing assays. (B) The transwell assays showed that knockdown of JARID2 expression inhibited HCCLM3 (B1) and MHCC97-H (B2) cells invasion, but JARID2 overexpression enhanced HepG2 cells (B3) invasion. (C) Immunofluorescence assays of cytoskeleton of HCCLM3control and HCCLM3shJARID2-1 (C1), MHCC97-Hcontrol and MHCC97-HshJARID2-1 (C2), HepG2Vector and HepG2JARID2 cells (C3). F-actin filaments were visualized in cells using rhodamine-phalloidin. (D) The HCC metastatic mouse model was constructed by using HCCLM3 and MHCC97-H cells transfected with shJARID2-1 or control vector, and HepG2 cells transfected with JARID2 or control vector as described in the Materials and Methods. The size of liver tumors in each group was calculated and compared in HCCLM3 (D1), MHCC97-H (D2) and HepG2 (D3) cells. Scale bar, 1 cm. (E) Representative pictures for intrahepatic (E1) and lung metastasis (E2). (F) The number of metastatic nodules per liver or lung was calculated and compared between HCCLM3control and HCCLM3shJARID2-1 (F1), MHCC97-Hcontrol and MHCC97-HshJARID2-1 (F2), HepG2Vector and HepG2JARID2 cells group (F3, F4). *P < 0.05; **P < 0.01; ***P < 0.001.