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. Author manuscript; available in PMC: 2013 Nov 15.
Published in final edited form as: Cancer Res. 2013 Mar 27;73(10):3041–3050. doi: 10.1158/0008-5472.CAN-12-3947

Figure 2.

Figure 2

HMGA2 is required for embryonic rhabdomyosarcoma growth in vitro. A, knockdown of HMGA2 in RD cells using lentiviral-based shRNAs. NT shRNA control or 3 independent shRNAs (1#, 2#, 3#) targeting HMGA2 were used. All 3 HMGA2 shRNAs significantly reduced HMGA2 levels, in comparison to the NT shRNA. B, knockdown of HMGA2 in ERMS cells reduces proliferation and induces cell death. Images were taken 96 hours after infection. Scale bar, 100 μm. C, knockdown of HMGA2 in ERMS cells reduces proliferation, measured by cell-titer assays. *, P < 0.05, Student t test. D, knockdown of HMGA2 in ERMS cells induces apoptosis, measured by activated caspase 3/7 activity. *, P < 0.05, Student t test, sh-HMGA2 sample versus sh-NT sample. E, overexpression of HMGA2 significantly rescues the apoptosis effect of HMGA2 shRNA. *, P < 0.05, Student t test.