Fig. 9: Effects of b-AP15 on tumor growth in vivo. | Cell Death & Disease

Fig. 9: Effects of b-AP15 on tumor growth in vivo.

From: USP14 and UCHL5 synergistically deubiquitinate PKCα and translocate NF-κB to promote the progression of anaplastic thyroid cancer

Fig. 9

A The images of tumors from nude mice treated with vehicle and b-AP15. B Time-dependent changes in tumor volume in nude mice treated with vehicle and b-AP15. (n = 6). C Quantification of tumor weight in nude mice treated with vehicle and b-AP15. (n = 6). D Body weight of nude mice over time in the control and b-AP15 groups. (n = 6) E H&E staining of heart, liver, spleen, lung, and kidney tissues from nude mice treated with vehicle and b-AP15. Scale bar, 100 μm. F. IHC staining of Ki67, PKCα, and p-P65 in tumor tissues from nude mice treated with vehicle and b-AP15. Scale bar, 50 μm. G Schematic representation of the USP14 and UCHL5 roles in normal thyroid cells and ATC cells. In normal thyroid cell, PKCα is ubiquitinated and degraded via the 26S proteasome, leading to transcriptional repression of C-MYC and BCL-XL. In ATC cell, PKCα is stabilized by USP14 and UCHL5, leading to the activation of NF-κB and subsequent transcriptional activation of C-MYC and BCL-XL.

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