Fig 2: Expression of MTA1 and EpCAM in tissue microarray samples. a The immunohistochemistry results showed that MTA1 were overexpressed in lung cancer tissues when compared with nonneoplastic tissues (*p < 0.05).b The immunohistochemistry results showed that EpCAM were overexpressed in lung cancer tissues when compared with nonneoplastic tissues (*p < 0.05). c Representative images showing immunohistochemical expression in lung cancer tissue specimens of MTA1 and EpCAM. Cases with strong and weak expression are represented. Original magnification, ×200

Fig 3: MTA1 could upregulate EpCAM expression and promote invasion and migration via upregulation of EpCAM expression in lung cancer cells. a Western blot analysis of the expression level of EpCAM in MTA1-overexpressing or MTA1-silencing cells. shNC: A549, PC-9, NCI-H446 cells transfected with Lenti-shNC-GFP; shMTA1: A549, PC-9, NCI-H446 cells transfected with Lenti-shMTA1; NC: A549, PC-9, NCI-H446 cells transfected with Lenti-NC-GFP. MTA1: A549, PC-9, NCI-H446 cells transfected with Lenti-MTA1. b Images of the transwell invasion assay in NC cells, MTA1-overepressed cells transfected with Scramble siRNA or EpCAMsiRNA and MTA1-silenced cells transfected with vector control or EpCAM. c Quantitative analysis of the number of invasion cells in the five groups of cells. The invaded cells were counted under × 200 magnification (five randomly selected fields). First, the number of invasive shMTA1 cells was significantly reduced (*p < 0.05, shMTA1 vs. shNC), and the number of invasive MTA1 cells was dramatically increased (*p < 0.05, MTA1 vs. NC). Second, invasive response of MTA1-overexpression cells was impaired significantly after downregulatingEpCAM (*p < 0.05, EpCAMsiRNA vs. Scramble siRNA in MTA1-overexpression cells), and invasion could be rescued by overexpressing EpCAM (*p < 0.05, EpCAM vs. Vector control in MTA1-silencing cells). d Representative images of the five cell groups in the wound healing assay (magnification,×200). e Quantitative analysis of the migration ability of lung cancer cells. First, the MTA1-silencing could reduce cells motility when compared with the negative controls cells (*p < 0.05, shMTA1 vs. shNC), and the MTA1-overexpression could increase cells motility when compared with the negative controls cells (*p < 0.05, MTA1 vs. NC). Second, a knockdown of EpCAM expression in MTA1-overexpression cells could dramatically attenuate cell migration (*p < 0.05, EpCAMsiRNA vs. Scramble siRNA in MTA1-overexpression cells), and the upregulation of EpCAM in MTA1-silencing cells could regain cell migration (*p < 0.05, EpCAM vs. Vector control in MTA1-silencing cells). All experiments were repeated three times

Fig 4: Enhanced expression of STIM1 in IBD patients. (A) Protein expression of STIM1 in inflammatory and matched-adjacent normal intestinal tissues from IBD patients. (B–D) IHC staining and IHC scores showing STIM1 expression in IECs and LP of IBD patients (n = 25). Scale bars: 100 µm, boxed pullout: 50 µm. Twenty-five random numbers between 0 and 0.2 were generated and added to the IHC score of each sample to avoid an overlap of points. (E) Representative immunofluorescence of CD45 (green) and STIM1 (red) in intestinal tissues from IBD patients. Scale bars: 100 µm. (F) Representative immunofluorescence of EpCAM (green) and STIM1 (red) in intestinal tissues from IBD patients. Scale bars: 100 µm. The results are presented as the means ± SEM. ****P < .0001, **P < 0.01, and *P < .05. (C and D) Paired Student t test for IHC scores without random numbers. DAPI, 4',6-diamidino-2-phenylindole.

Fig 5: MTA1 expression positively correlates with EpCAM expression in lung cancer patients. Statistics were calculated using Spearman testing. *, p < 0.01