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. 2015 May 14;10(5):e0127239. doi: 10.1371/journal.pone.0127239

Fig 2. Inactivation of p65 reduces the abilities of in vitro colony formation, in vivo tumor formation, migration, invasion, and angiogenesis in NPC.

Fig 2

(A) Western blot analysis shows the expression of exogenous IκBα-SR with triple HA-tag (^) in HONE1 cells. The p84 served as a loading control. (B) 2D colony formation assay shows that IκBα-SR suppressed the colony-forming ability of HONE1 cells compared to pWPI-vector alone (VA). Bar graphs indicate data obtained from an average of triplicate experiments ± S.E.M. (C) Nude mice were inoculated subcutaneously with IκBα-SR and pWPI-VA HONE1 cells. IκBα-SR-transduced cells showed delayed and reduced tumor growth kinetics compared to pWPI-VA. Each data point represents an average tumor volume of six injection sites inoculated for each cell population ± S.E.M. (D) Wound healing analysis for pWPI-VA and IκBα-SR showed delayed migration of IκBα-SR cells compared to VA. Bar graphs show the percentage difference between IκBα-SR and VA cells ± S.E.M. (E) Migration chamber assays showed that IκBα-SR-expressing HONE1 cells reduced migration compared to VA cells. Data represented on the bar graph are the average of triplicate experiments ± S.E.M. (F) HUVEC tube formation was suppressed with IκBα-SR conditioned medium compared to that of VA cells. Data represented on the bar graph are the average of triplicate experiments ± S.E.M. The (*) for all graphs indicate P-value < 0.05.