Fig 2: SNHG1 increases SOCS2 expression and regulate the JAK/STAT signaling pathway in AGS cells (A) Hierarchically clustered heatmap of differentially expressed genes in SNHG1 overexpressing BGC-823 cells and control cells. (B) qRT-PCR analysis of differentially expressed genes in SNHG1 overexpressing BGC-823 cells and control cells and AGS cells transfected with siSNHG1 and siNC. (C) Western blots of SOCS2 and JAK/STAT signaling pathway proteins in SNHG1 overexpressing BGC-823 cells and control cells and AGS cells transfected with siSNHG1 and siNC. (D) Relative expression of SOCS2 in 98 paired GC tissues and adjacent noncancerous tissues. (E) Correlation analysis of the relationship between SNHG1 and SOCS2 expression levels in 150 GC tumor tissues. **p < 0.01 and ***p < 0.001.

Fig 3: TRIM6 may promote STAT3 phosphorylation via SOCS2. (A) Protein expression of STAT3 phosphatases (SHP-1, SHP-2), SOCS1, SOCS2, SOCS3, and PIAS1 in TRIM6 knockdown HCT116 cells. (B) SOCS2 mRNA expression level measured via qRT-PCR in TRIM6 knockdown HCT116 cells. SOCS2 protein (C) and mRNA expression levels (D) in TRIM6-overexpressed SW620 cells detected via Western blot and qRT-PCR, respectively. (E) CO-IP analysis between TRIM6 and SOCS2. (F) TRIM6 and SOCS2 expression levels in TRIM6-overexpressed SW620 cells with/without MG132 treatment. (G) IP analysis of SOCS2 ubiquitination in TRIM6 knockdown HCT116 cells. The results are from at least three separate experiments.

Fig 4: miR-196b interacted with SOCS2. (a) the binding site between SOCS2 and miR-196b is shown. (b) spearman correlation analysis revealed the negative correlation between miR-196b and SOCS2 expression. (c) the cell lysate was incubated with an anti-AGO2 antibody for RIP, and the SOCS2 content was measured by RT-PCR. (d) expression of SOCS2 mRNA was detected using qRT-PCR in TE-1 cells with upregulated or downregulated expression of miR-196b. (e) the expression of SOCS2 protein was measured using a western blot assay. (f) luciferase activity of WT-SOCS2 TE-1 cells group was weakened or enhanced by miR-196b overexpression or knockdown, respectively, but luciferase activity has no change in MUT-SOCS2 TE-1 cells by miR-196b. The above analysis was performed by graphpad prism software.***P < 0.001

Fig 5: miR-532-3p overexpression suppressed the proliferation, migration, and invasion of pancreatic cancer cells, as well as tumor formation in nude mice.(A, B, C) The effect of miR-532-3p knockdown or overexpression on the proliferation, migration, and invasion capacities of PC cells. (D) Tumor volume and weight of nude mice were evaluated after injecting with cells stably expressed miR-532-3p inhibitor or mimics. (E, F) The expression of DNMT3A and SOCS2 and the phosphorylation level of STAT5 were measured using qRT-PCR and/or Western blot in vivo. *P < 0.05, **P < 0.01, and ***P < 0.001.