Fig 1: Immunohistochemical staining for MYSM1 in human colorectal tissues.(A) Expression levels of MYSM1 in normal mucosa (n = 30) and primary carcinoma tissues (n = 30)from patients with CRC were detected by immunohistochemical staining (×10, 100 µm; ×40, 20 µm).(B)MYSM1 protein levels in normal mucosa and primary carcinoma tissues were quantified as shown as line chart.
Fig 2: Kaplan-Meier survival analysis in patients with CRC.Overall survival curves for patients according to the negative (n = 57) and positive (n = 66) expression levels of MYSM1 of immunohistochemical variables in tumor cells.
Fig 3: Western blot analysis for MYSM1 in human CRC tissues.(A) Expression levels of MYSM1 in normal mucosa, primary carcinoma, lymphnode metastasis tissues and liver metastasis tissues were examined by Western blot using the corresponding antibody.ß-actin was detected as internal reference.(B) The bar graph showed the amount of interest proteins normalized to the amount of ß-actin.*P < 0.05compared with normal mucosa, **P < 0.01 compared with primary carcinoma, mean ± SEM. N.S., no significance.
Fig 4: Immunohistochemical staining for MYSM1 in human CRC tissues.(A) Expression levels of MYSM1 in primary carcinoma (n = 30) and lymphnode metastasis tissues (n = 30)were detected (×10, 100 μm; ×40, 20 μm). (B)Expression levels of MYSM1 in primary carcinoma (n = 38) and liver metastasis tissues (n = 38) were examined (×10, 100 μm; ×40, 20 μm).
Fig 5: MYSM1 silencing decreases migration and invasion in CRC SW480 cells.(A) CRC SW480 cells were transfected with or without siRNA against MYSM1 (siMYSM1) or control siRNA (siCtrl). Western blot analysis was used to detect the interference efficiency of MYSM1 protein in cells.MYSM1 protein was examined using the corresponding antibody.β-actin was detected as internal reference.(B) The invasion abilities of MYSM1-silenced and non-silenced cells were evaluated by Transwell assay. (C)The migration abilities of MYSM1-silenced and non-silenced cells were evaluated by Scratch assay.
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