Decreased ST2 expression is associated with gastric cancer progression and pathogenesis.

Gastric cancer is a type of cancer with increasing incidence and high mortality rates, but molecular biomarkers of diagnostic and therapeutic value are currently lacking. The aim of the present study was to examine the expression pattern of the interleukin 1 receptor-like 1 (ST2) protein and assess its clinicopathological significance in gastric cancer. Western blot analysis of 12 gastric cancer specimens and paired adjacent tissues demonstrated that the protein levels of 2 isoforms of ST2, soluble secreted ST2 and the ST2 variant without the third immunoglobulin motif and splicing in the C-terminal, were markedly decreased in cancer tissues compared with non-cancerous tissues. Immunohistochemical analysis demonstrated that ST2 protein expression was markedly decreased in primary gastric cancer tissues (39.1%, 90/230) compared with adjacent non-cancerous tissues (60.7%, 54/89) (P<0.05). Statistical analysis demonstrated that decreased ST2 expression was significantly associated with advanced tumor node metastasis stage (P<0.001) and tumor differentiation (P<0.001). These data suggest that ST2 protein may be a valuable biomarker of gastric cancer progression and pathogenesis.

miR­29a­3p represses proliferation and metastasis of gastric cancer cells via attenuating HAS3 levels.

MicroRNA­29a (miR­29a) has recently been in the spotlight as a tumor suppressor whose encoding gene is frequently suppressed in cancers. The aim of the present study was to investigate the biological functions and underlying molecular mechanism by which miR­29a­3p suppresses gastric cancer peritoneum metastasis. Cell proliferation, colony­forming, wound healing and Transwell migration assays were performed in the present study. MiR­29a­3p expression was markedly decreased in gastric cancer cell lines with stronger metastatic potential. Silencing miR­29a­3p expression promoted gastric cancer cell proliferation, colony­forming, migration and invasion. By contrast, overexpression of miR­29a­3p inhibited these biological phenotypes. In addition, it was revealed that miR­29a­3p functioned through downregulating hyaluronan synthase 3 expression. Collectively, dysregulated miR­29a­3p expression in gastric cancer cells was associated with malignant properties primarily relevant to migration and metastasis. The results suggest that miR­29a­3p may be a potential therapeutic target for gastric cancer.

MicroRNA-214 promotes peritoneal metastasis through regulating PTEN negatively in gastric cancer.

BACKGROUND AND OBJECTIVE: We aimed to investigate the effects of microRNA-214 (miR-214) on peritoneal metastasis as well as to elucidate its regulatory mechanism in gastric cancer (GC). METHODS: The expression levels of miR-214 in human GC cell lines MKN-28NM, MKN-28M, GC9811 and GC9811-P were analyzed by quantitative real-time PCR. Lentiviral miR-214, lentiviral miR-214 inhibitor, and empty lentiviral vector were transfected to GC cell lines, respectively. The roles of miR-214 in cell invasion, migration, proliferation and colony-forming ability were then analyzed. Besides, the expression levels of PTEN in different transfected cells were determined by western blot analysis. RESULTS: We found that miR-214 was up-regulated in GC9811-P cells with high metastatic potential to the peritoneum compared with that in GC9811 cells. In addition, in vitro overexpression of miR-214 promoted cell invasion, migration, proliferation and colony-forming ability of GC9811 cells, while down-regulation of miR-214 had opposite effects in GC9811-P cells. Besides, overexpression of miR-214 in GC9811 cells markedly down-regulated PTEN expression, whereas down-regulation of miR-214 in GC9811-P cells significantly increased PTEN expression. CONCLUSIONS: Our findings indicate that miR-214 may promote peritoneal metastasis of GC cells via down-regulation of PTEN, thus leading to the progression of GC.