ABSTRACT
Galectin-1 (Gal1) and non-SMC condensin I complex, subunit G (NCAPG) are associated with metastasis in several malignant tumors. However, their precise roles in gastric cancer (GC) remain uncertain. This study explored the clinical significance and relationship of Gal1 and NCAPG in GC. Gal1 and NCAPG expressions were significantly up-regulated in GC compared to adjacent non-cancerous tissues by immunohistochemistry (IHC) and Western blotting. Besides, methods including stable transfection, quantitative real-time reverse transcription PCR, Western blotting, Matrigel invasion and wound-healing assays in vitro, were also conducted. IHC scores for Gal1 and NCAPG had a positive correlation in GC tissues. High Gal1 or NCAPG expression significantly correlated with poor prognosis in GC, and Gal1 combined with NCAPG had a synergetic effect on the prediction of GC prognosis. Gal1 overexpression in vitro enhanced NCAPG expression, cell migration, and invasion in SGC-7901 and HGC-27 cells. Simultaneous Gal1 overexpression and NCAPG knockdown in GC cells partly rescued the migrative and invasive abilities. Thus, Gal1 promoted GC invasion through increased NCAPG expression. The present study demonstrated the prognostic significance of the combination of Gal1 and NCAPG in GC for the first time.
Subject(s)
Stomach Neoplasms , Humans , Stomach Neoplasms/pathology , Galectin 1/genetics , Galectin 1/metabolism , Prognosis , Cell Movement/genetics , Cell Proliferation , Gene Expression Regulation, Neoplastic , Cell Line, Tumor , Cell Cycle Proteins/metabolismABSTRACT
Right hemicolectomy for colon cancer may be complicated by leaks, stenoses, or fistulas. These complications usually occur at the ileocolic anastomosis and can be managed endoscopically. However, fistulas that are large cannot be managed by endoscopy and require surgical intervention. After laparoscopic radical right hemicolectomy, duodenal fistulae is relatively rare. Among duodenal fistulae, internal duodenocolic fistulae is relatively common, but duodeno-ileum fistulae is extremely rare. Here, we report a case of duodeno-distal ileum fistula after right hemicolectomy with short bowel syndrome, that was surgically treated. After surgical treatment, the symptoms of short bowel syndrome disappeared, weight gain was obvious, and the clinical effect was satisfactory.
ABSTRACT
Background The gastric cancer (GC) microenvironment has important effects on biological behaviors, such as tumor cell invasion and metastasis. However, the mechanism by which the GC microenvironment promotes GC cell invasion and metastasis is unknown. The present study aimed to clarify the effects and mechanism of galectin-1 (GAL-1, encoded by LGALS1) on GC invasion and metastasis in the GC microenvironment. Methods The expression of GAL-1/ LGALS1 was determined using western blotting, immunohistochemistry, and quantitative real-time reverse transcription PCR in GC tissues. Besides, methods including stable transfection, Matrigel invasion and migration assays, and wound-healing assays in vitro; and metastasis assays in vivo, were also conducted. Results GAL-1 from cancer-associated fibroblasts (CAFs) induced the epithelial-mesenchymal transition (EMT) of GC cells though the transforming growth factor beta (TGF-ß1)/ Sma- and mad-related protein (Smad) pathway, and affected the prognosis of patients with GC. The level of GAL-1 was high in CAFs, and treating MGC-803 and SGC -7901 cell line with the conditioned medium from CAFs promoted their invasion and metastasis abilities. Overexpression of LGALS1 promoted the expression of TGF-ß1 and induced EMT of GC cell lines. A TGF-ß1 antagonist inhibited the invasion and migration of GC cells. In vivo, overexpression of LGALS1 promoted GC growth and metastasis, and the TGF-ß1 antagonist dramatically reversed these events. Conclusions These findings suggested that high expression of GAL-1 in the GC microenvironment predicts a poor prognosis in patients with GC by promoting the migration and invasion of GC cells via EMT through the TGF-ß1/Smad signaling pathway. The results might provide new therapeutic targets to treat GC.
