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. 2021 Nov 19;49(21):12211–12233. doi: 10.1093/nar/gkab1122

Figure 4.

Figure 4.

Inhibition of HCI-002 PDX tumor growth and metastasis by JQ1 and EZM2302. (A) A schematic of the workflow treating HCI-002 xenografts with vehicle, JQ1, EZM2302, or both. (B) Representative tumors in vehicle, JQ1, EZM2302 or both treatment groups (Top). Growth curves (bottom) show the tumor volumes normalized by the pre-drug treated tumor volumes. **P< 0.01; *P< 0.05. (C) Gene set enrichment analysis (GSEA) of RNA-seq data (n = 3) from tumors treated with JQ1, TP-064 or JQ1 and TP-064 in combination on 125 SEs signature genes. (D) Real-time qPCR analyses of SE-regulated genes after treatment with vehicle, JQ1, EZM2302 or both in HCI-002 PDX. (E) Western blotting of SE-regulated oncoproteins after treatment with indicated drugs in HCI-002 PDX. (F) Ki67 (upper left) and me-BAF155 (lower left) IHC staining in vehicle, JQ1, EZM2302 or both treated HCI-002 tumors. Ki67-positive cells under each treatment condition were plotted (right). Data are mean ± s.d. **P< 0.01. (G) Detection of lymph node micrometastasis by IHC using human specific mitochondria antibody (upper left) with HCI-002 tumors. IgG serves as a negative control (lower left). Micrometastatic cancer cells in lymph nodes were quantified under each treatment conditions (right). Data are mean ± s.d. **P< 0.01; *P< 0.05.