Fig. 5

Signaling pathways involved in BMP4-activated autophagy to promote HCC proliferation: a Western blot was applied to detect the expression of JNK1, p-JNK, Bcl-2 and p-Bcl-2 in HepG2 and HCCLM3 cells. HCC cells were appointed to the indicated treatment respectively. b The effect of JNK inhibitor SP600125 was determined by Western blot in HepG2 and HCCLM3 cells. c Western blot was performed to detect the expression of LC3-II, p62 and BECN1 in HCC cells. JNK pathway inhibition significantly attenuated the BMP4-activated autophagy in HepG2 and HCCLM3 cells. d Quantification of LC3-II expression level by densitometric analysis and was normalized to the control (blank) groups. GAPDH was used as the internal control. n = 3, one-way ANOVA with post-hoc Tukey’s test. e Effects of JNK inhibitor SP600125 on long term colony formation promoted by BMP4 in HCC cells. JNK pathway inhibition significantly attenuated the promotion effects on the number of colonies both in HepG2 and HCCLM3. n = 3, one-way ANOVA with post-hoc Tukey’s test. f Effects of JNK inhibitor SP600125 on BMP4-promoted HCC cells growth. JNK pathway inhibition significantly attenuated the promotion effects on the cell viability both in HepG2 and HCCLM3