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. Author manuscript; available in PMC: 2020 Jan 1.
Published in final edited form as: Mol Cancer Ther. 2018 Oct 18;18(1):51–61. doi: 10.1158/1535-7163.MCT-18-0104

Figure 5: G2.2 inhibits colon CSCs in vivo through p38 activation-dependent mechanism.

Figure 5:

(A) Average tumor volume of Dual hi HT-29 induced s.c. xenografts treated with 1. Veh, 2. G2.2 (schedule), 3. SB (schedule) (p38 α/β inhibitor) 4. SB 3-hours prior to G2.2 (SG) indicates reversal of tumor volume inhibition induced by G2.2 in the presence of pre-treatment with SB. (B) G2.2 induced inhibition of CSC self-renewal (3° sphere formation) in xenograft-derived cells was almost completely reversed by pre-treatment with SB. Interestingly, treatment with SB alone resulted in increase in CSC self-renewal despite modest tumor volume reduction suggesting a role of p38 in inversely regulating CSCs. (C) Flow cytometry analysis (bar-graph representation) of the proportion of Dual (hi) cells in xenografts demonstres the role of SB in reversing the CSC inhibition by G2.2. (D) Western blot analyses and the corresponding bar graph representation of relative densitometry values normalized to GAPDH (housekeeping protein) of CSC (CD133, LGR5)/ self-renewal (BMI1) markers as well as pp38 levels shows complete reversal of G2.2’s effects in mice treated with SB>G2.2 treatment. Error bars represent ±1 SEM. *p-value < 0.05 compared to vehicle treated control. p-value <0.005 compared to vehicle. §p-value < 0.005 compared to G2.2.