Skip to main content
. Author manuscript; available in PMC: 2013 Jul 1.
Published in final edited form as: Free Radic Biol Med. 2012 May 9;53(1):44–50. doi: 10.1016/j.freeradbiomed.2012.04.031

Fig. 1. SOD2 overexpression is related to the migration and invasion of TSCC.

Fig. 1

(A) The migration ability of TSCC cells was assessed using a wound healing assay. The confluent monolayer was “wounded” and allowed to migrate for 24 h. Quantification of distance migrated from time 0 to 24 h was calculated (n = 6). UM1 cells displayed significantly more migration than UM2 or Tca8113. *: P< 0.05.

(B) The invasion ability of TSCC cells was assessed by a transwell invasion assay. Cells were seeded in a BD Biocoat Matrigel invasion chamber and allowed to invade through the Matrigel toward the lower chamber for 24 h. The number of cells invading through the chamber was quantified. UM1 cells displayed a significantly higher invasion rate than UM2 or Tca8113. *: P< 0.05.

(C) Levels of SOD2 protein and activity were assessed by western blot and SOD activity assay, respectively. Significant increases in SOD2 protein levels and activities were observed in UM1 cells compared to UM2 or Tca8113 cells. *: P< 0.05.

(D) Levels of CAT (catalase) protein and activity were assessed by western blot and CAT activity assay, respectively. CAT protein levels and activities were not difference between UM1 and UM2 cells.

(E) H2O2 concentrations were measured as described in the Materials and Methods section. UM1 cells displayed significantly higher H2O2 production compared to UM2 cells. *: P< 0.05.

(F) Cell proliferation was measured using an MTT assay. The cell proliferation rate of UM1 was significantly higher than UM2. *: P< 0.05.