Fig 2: A directly positive correlation between TESC and c-Fos in TPC-1 and BHT101 cells. The mRNA and protein level of c-Fos were determined after the expression of TESC was downregulated and upregulated in TPC-1 and BHT101 cells respectively. A The relative mRNA level of c-Fos was detected using qRT-PCR after the inhibition of TESC in TPC-1 and BHT101 cells. B The relative protein level of c-Fos was shown as a bar graph after the inhibition of TESC in TPC-1 and BHT101 cells. C The proteins expression of c-Fos was examined by western blot assay after the inhibition of TESC in TPC-1 and BHT101 cells. D The relative mRNA level of c-Fos was detected using qRT-PCR after the overexpression of TESC in TPC-1 and BHT101 cells. E The relative protein level of c-Fos was shown as a bar graph after the overexpression of TESC in TPC-1 and BHT101 cells. F The proteins expression of c-Fos was examined by western blot assay after the overexpression of TESC in TPC-1 and BHT101 cells. Data in qRT-PCR assay were expressed after being normalized to GAPDH. Data in western blot assay were expressed after being normalized to ß-actin. The means ± SD of three independent samples were shown. *p < 0.05

Fig 3: GO and KEGG enrichment analysis of TPC-1 and BHT101 cells transfected with TESC-RNAi. The target RNAi sequences of TESC was cloned into GV493 vector, and then were transfected into TPC-1 and BHT101 cells using Polybrene, respectively. Subsequently, TPC-1 and BHT101 cells were executed the transcriptome sequencing. A and B GO enrichment analysis of DEGs in TPC-1 and BHT101 cells, respectively. C KEGG enrichment analysis of an intersection of TPC-1 and BHT101 cells

Fig 4: TESC interacted with c-Fos through ERK1/2 in TPC-1 and BHT101 cells. A The relative protein level of ERK1/2 and phosphorylated ERK1/2 was examined by western blot assay in TPC-1 and BHT101 cells treated with TESC-RNAi or FOS-RNAi. B The relative protein level of ERK1/2 and phosphorylated ERK1/2 was shown as a bar graph in TPC-1 and BHT101 cells treated with TESC-RNAi or FOS-RNAi. C Overexpressed plasmid of TESC was transfected into TPC-1 and BHT101 cells, and then cells were treated with ERK inhibitor AG-126. The proteins expression of c-Fos, ERK1/2 and phosphorylated ERK1/2 was examined by western blot assay. D The relative protein level of c-Fos, ERK1/2 and phosphorylated ERK1/2 was shown as a bar graph. Data in western blot assay were expressed after being normalized to ß-actin. The means ± SD of three independent samples were shown. *p < 0.05

Fig 5: TESC effectively promoted the proliferation, migration, invasion, and inhibited the apoptosis of PTMC. A The expression of TESC in PTMC tissues and PTMC-adjacent tissues was detected by IHC, and the expression change of TESC was statistically analyzed. B The mRNA expression of TESC in the cells was detected using qRT-PCR. C Three target RNAi sequences of TESC were cloned into GV493 vector, and then were transfected into TPC-1 and BHT101 cells using Polybrene, respectively. The interference efficiency was determined by qRT-PCR. D and E The effect of TESC on the proliferation of TPC-1 and BHT101 cells was detected by CCK8 and colony formation assay. F The apoptosis rate of TPC-1 and BHT101 cells was determined by flow cytometric assay. G The effect of TESC on the migration of TPC-1 and BHT101 cells was examined by scratch test. H The effect of TESC on the invasion abilities of TPC-1 and BHT101 cells was examined by transwell assay. I and J TESC-RNAi transfected (a total of 2 × 106) or control cells were subcutaneously injected into the flanks of nude mice. Tumor volume and weight were measured. K The level of Ki-67 was detected by IHC after the inhibition of TESC. The means ± SD of three independent samples were shown. *p < 0.05