Skip to main content
. 2019 Oct 31;8(11):1360. doi: 10.3390/cells8111360

Figure 4.

Figure 4

Loss of HOXA9 inhibited apoptosis, promoted autophagy and tumor growth in vivo. (a) HOXA9 depletion enhances xenografts growth. Statistical data of tumor volumes represent the average of three independent experiments ± s.d, respectively. (b) Dissected xenografts from three sacrificed mice were imaged at the end of experiment. Black arrows point the siNC-treated xenografts while white arrows indicate siHOXA9-treated xenografts. (c) The expression of HOXA9, RELA, BCL-XL, ULK1, ATG3, and ATG12 was detected in the dissected xenografts by qRT-PCR. Statistical data of qRT-PCR represent the average of three independent experiments ± s.d. (d) The protein expression levels of HOXA9, RELA (p65), BCL-XL, ULK1, ATG3, and ATG12 was detected in xenografts after siHOXA9 treatment by western blot. (e) Histopathology analysis (IHC staining) of HOXA9, RELA (p65), BCL-XL, ULK1, ATG3, and ATG12 on tumor sections. Scale bar, 100 µm. (f) A model of the HOXA9-NF-κB regulatory axis in cSCC development. In cSCC tumors, loss of HOXA9 up-regulates NF-κB and its downstream anti-apoptotic gene BCL-XL and pro-autophagic genes of ULK1, ATG3, and ATG12, which contributes to the repressed apoptosis, enhanced autophagy and promotes cSCC progression. * p < 0.05, ** p < 0.01.