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. 2022 Sep 9;60(1):1710–1720. doi: 10.1080/13880209.2022.2112963

Figure 5.

Figure 5.

MSN inhibited APS-mediated antitumor effect via maintaining PD-L1 stability. SMMC-7721 and Huh-7 cells were respectively pre-treated with 0.1 mg/mL, 0.5 mg/mL and 1 mg/mL of APS for 4 h, and APS-treated cells were treated with 10 ng/mL IFN-γ for 24 h. (A) MSN and p-MSN levels were measured by Western blot. (B) The combination of MSN and PD-L1 was verified by co-IP assay. sh-MSN#1 and sh-MSN#2 vectors were transfected into SMMC-7721 and Huh-7 cells at 48 h for MSN inhibition, sh-NC vector served as the negative control, and MSN inhibited SMMC-7721 and Huh-7 cells were treated with cycloheximide (50 μg/mL) at 0 h, 4 h, 8 h, 12 h, 24 h. (C) PD-L1 and MSN protein levels were measured by Western blot after MSN inhibition. Treated-SMMC-7721 and Huh-7 cells were transfected with wild type MSN (WT-MSN), non-phosphorylated MSN (T558A-MSN) and phosphorylated MSN (T558D-MSN) vectors. (D) MSN protein level was measured by Western blot. (E) SMMC-7721 and Huh-7 cell apoptosis was evaluated by flow cytometry. The data were expressed as mean ± SD. All data were obtained from at least three replicate experiments (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001.