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. 2022 Jul 11;13(7):593. doi: 10.1038/s41419-022-05026-x

Fig. 3. STAT1 downregulation by LSECtin is involved in GC cell adhesion and migration.

Fig. 3

A The expression of STAT1 in GC cells treated with 0.5, 1, and 5 μg/ml LSECtin protein and control IgG for 12 h was detected by Western blot analysis. B, C The expression of p-STAT1 and STAT1 protein in gastric cancer (GC) cells treated with 5 μg/ml LSECtin protein and control IgG for 24 h was detected by Western blot analysis (B). Semiquantitation of the phosphorylation level of STAT1 and STAT1 protein was from Western blot analysis (C). D STAT1 expression levels in 415 samples of GC and 35 samples of normal tissue, STAT1 expression levels in 32 tumor and matched normal samples from GC patients, STAT1 expression levels in M0 and M1 gastric tumors from TCGA were analyzed, and survival analysis curves were generated from 876 GC patients using the Kaplan-Meier plotter database. M0, no distant metastasis; M1, distant metastasis. E Wound healing assays of GC cells with LSECtin treatment, STAT1 knockdown or overexpression and the distance between the edges of the scratch was quantified using ImageJ software. F The effect of LSECtin on STAT1 knockdown or overexpression GC cells migration were examined with Transwell migration assays, and the number of migrated cells was counted by ImageJ software. G The effect of LSECtin on STAT1 knockdown or overexpression GC cells migration were examined with EdU experiments. H Adhesion between GC cells and frozen mouse lymph node sections was detected in vitro by H&E staining (left). The right panel shows the cell number. Error bars indicate standard deviation (n = 3). Data, the means ± SD.