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Figure 7 | Molecular Cancer

Figure 7

From: GPCR-like signaling mediated by smoothened contributes to acquired chemoresistance through activating Gli

Figure 7

JNK is involved in maintaining the chemoresistance of K562 cells with forced expression of SmoA1 by activating Gli. A, K562 cells with forced expression of GFP, SmoA1 or SmoA1 plus JNK1(APF) by lenti-virus approach were collected for immunoblotting of phosphorylation of JNK and c-Jun. GAPDH were used as a loading control. B-D, Ectopic expression of SmoA1 causes K562 cells resistant to anti-cancer drugs Dox (B), VP-16 (C), and Imatinib (D), while JNK dominant negative mutant JNK1(APF) abolishes these resistances. K562 cells with forced expressions of GFP, SmoA1 or SmoA1 plus JNK1(APF) by lenti-virus approach were seeded in 96 well plates, and were incubated with or without Dox, VP-16, and Imatinib for 72 h. Data are shown as mean ± s.d. from three separated experiments. E, K562 cells with forced expressions of GFP, SmoA1 or SmoA1 plus JNK1(APF) by lenti-virus approach were harvested for QT-PCR analysis of the expression of Gli1 at mRNA level.

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