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. 2023 Mar 31;13(6):2645–2662. doi: 10.1016/j.apsb.2023.03.025

Figure 5.

Figure 5

IL4/IL13 induces miR-660-5p expression by activating STAT6 pathway. (A–C) THP-1-derived TAM was treated with indicated dose of IL4, IL13, IL6, IL10 and TGF-β for 48 h. RT-PCR was performed to detect the expression of miR-660-5p. (D–H) THP-1-derived TAM was treated with indicated dose of STAT3 inhibitor (STAT3i) or STAT6 inhibitor (STAT6i) for 2 h, and then treated with 20 ng/mL of IL4 or IL13 for 48 h. RT-PCR was performed to detect the expression of miR-660-5p in TAM (D, F) and TAM-exosome (H). STAT3, p-STAT3, STAT6 and p-STAT6 protein levels were detected by Western blot (E, G). (I–L) miR-660-5p levels were detected in PBMC or THP-1-derived M0, M2 and TAM by RT-PCR (I, K). STAT6 and p-STAT6 protein levels were detected by Western blot (J, L). (M–P) HeLa alone or mixed with TAM cells were injected into nude mice (n = 5). Nude mice were administered with ERA and STAT6i as indicated at each time point. Tumor volume was measured once per 2–3 days by using calipers for 30 days (M, N). Change in mice body weight was displayed (O, P). The relative quantification of protein was analyzed by scanning densitometry using Image J software and β-actin was used as the loading control. Data are represented as the mean ± SEM of three replicates. For mice model studying, data are represented as the mean ± SEM of 5 mice. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 compared to control.