Fig 2: Schematic illustration of STC2-promoted EMT process through activation of AKT and ERK signaling pathways

Fig 3: STC2 promotes colorectal cancer tumorigenesis in vitro and in vivoCell proliferation, invasion and migration were greatly increased or decreased in STC2-overexpressing (A–C) or STC2-knockdown (D–F) HT29 cells. Cell migration and cell invasion was observed at 24, 48 h after transfection with pTango-STC2 plasmid (A-C) or STC2 siRNA (si-STC2) (D-F). The average values ± SEM was obtained from three separate experiments. **P < 0.01, ***P < 0.001. (G) The tumors isolated from xenograft nude mice (n = 6), which were injected with STC2-overexpressing HT29 cells, were much bigger than the control group injected with pTango-containing HT29 cells. After the tumor growth for 20 days (cell injection for 30 days), nude mice were killed to isolate tumor. (H) Tumor growth curves of xenograft nude mice. HT29-STC2:STC2-overexpressing HT29 cells. HT29-ctrl: pTango-containing HT29 cells, the control group. The average values ± SEM were calculated from three separate experiments. *P < 0.05, **P < 0.01, ***P < 0.001. (I) The average weight of the dissected tumors was much heavier than the control group (n = 6).

Fig 4: STC2 promotes EMT process via AKT and ERK signaling pathwaysEMT markers and the related PI3K/AKT, MEK/ERK signaling molecules were significantly changed in NCM460 cells incubated with the exogenous STC2 protein (STC2) (A) and transiently transfected with pTango-STC2 plasmids (pTango-STC2) (B). Conversely EMT markers and PI3K/AKT, MEK/ERK signaling molecules were oppositely changed in EMT cells treated with STC2 siRNA (si-STC2) for 48 h (C).

Fig 5: Serum STC2 level correlated with tumor stage and overall survival for colorectal cancer patients(A) The secretion levels of serum STC2 were compared between colorectal cancer (CRC) patients and normal person by western blot. Normal: sera from the health donor; Case1-3: 3 cases of CRC sera. Reversible Ponceau staining was used as a loading control. (B) The mean serum STC2 level of CRC patients (n = 77) was much higher than health donors (n = 14) (P < 0.001). (C) Comparison of serum STC2 level in CRC patients with TNM stage I-II versus those with stage III–IV. (D) Kaplan-Meier overall survival curves for CRC patients based on serum STC2 levels. The overall survival rate for patients with low serum STC2 level was significantly higher than those of patients with high serum STC2 level (P < 0.05). The low serum STC2 level was defined as less than 1179.35 pg/mL (median value) (average 834.92 ± 242.55 pg/mL), while the high serum STC2 level was above 1179.35 pg/mL (average 1463.61 ± 241.70 pg/mL). (E) A ROC analysis was performed based on the ELISA results. Empirical ROC curves deviated from typical ROC-curve shapes, and a portion of the curve leading to the northeast corner of the ROC space had relatively steep and constant slopes. AUC: area under the ROC curve.