lncRNA can serve as a miRNA sponge and block the function of miRNA. High expression of lncRNA SNHG16 (small nucleolar RNAhostgene16) was discovered in gastric cancer (GC) and many other tumors. However, the mechanism of SNHG16 in GC is still unclear. In this research, we detected the expression level of SNHG16 in GC tissues and cell lines by qRT-PCR and FISH assay. RIP and Dual Luciferase Reporter Assay revealed that miR-135a is a target of SNHG16. SNHG16 gene knockdown experiment indicated that the expression level of SNHG16 can influence GC cells proliferation, colony formation, invasion ability and apoptosis in a miR-135a dependent manner. Western Blot assay showed that knockdown of SNHG16 decreased the expression of JAK2 and p-STAT3 in GC cells while miR-135a can offset the facilitated impact. Then the expression level of SNHG16 and miR-135a in the si-STAT3 GC cells was detected by qRT-PCR and the results showed that SNHG16 may be a target gene of p-STAT3. Collectively, it was suggested that SNHG16 can serve as a miR-135a sponge and block the function of miR-135a in JAK2/STAT3 pathway.

In this work, we aimed to determine the expression and biological functions of microRNA (miR)-577 in colorectal cancer (CRC). The results showed that miR-577 was downregulated in CRC specimens and cell lines. Restoration of miR-577 significantly suppressed the proliferation and colony formation and induced a G0/G1 cell cycle arrest in CRC cells. 5-Fluorouracil (5-FU)-resistant SW480 cells (SW480/5-FU) were found to have elevated levels of miR-577. Ectopic expression of miR-577 enhanced 5-FU sensitivity in SW480/5-FU cells. Heat shock protein 27 (HSP27) was identified as a target gene of miR-577. Enforced expression of HSP27 reversed the effects of miR-577 on CRC cell growth and 5-FU sensitivity. Xenograft tumors derived from miR-577-overexpressing SW480 cells exhibited significantly slower growth than control tumors. In conclusion, our results support that miR-577 acts as a tumor suppressor in CRC likely through targeting HSP27. Therefore, miR-577 may have therapeutic potential in the treatment of CRC.

Although the clinicopathological features of cardia gastric cancer (GC) differ from those of non-cardia GC, it is unclear whether the former has poorer prognosis than the latter. The aim of this study was to compare clinicopathological characteristics and prognosis between cardia and non-cardia GC. From December 2009 to December 2011, 1633 patients who had undergone R0 resection of GC at four Chinese centers were enrolled in this study. Their clinicopathological features and survival outcomes were evaluated. Compared with non-cardia GC, cardia GC was associated with a significantly higher proportion of male patients, older age, more advanced pathological stage, and less-favorable clinicopathological features at diagnosis. The 5-year survival rate was significantly lower in the cardia GC group than in the non-cardia GC group. However, no significant difference in overall survival (OS) was observed between the two groups at any pathological TNM stage. Pathological stage was confirmed as an independent prognostic factor of OS. More advanced disease represents most of the cases in this Chinese population. Compared with patients with non-cardia GC, patients with cardia GC were diagnosed at a more advanced stage and had worse prognosis after undergoing R0 resection. However, cardia and non-cardia GCs have similar stage-for-stage prognoses.

The positive status of HER2 based on IHC staining was not related to the survival in patients with GC among the Chinese population.

Background: Polyphyllin I, a bioactive phytochemical extracted from Rhizoma Paridis, has been reported to exhibit anticancer activity. However, little is known about the potential of Polyphyllin I in induction of gastric cancer (GC) cell apoptosis and its underlying mechanisms. Methods: Dual-luciferase reporter assay was performed to test the bioactivity of Polyphyllin I on inhibiting JAK2/STAT3 signaling pathway. The anti-proliferation activity of Polyphyllin I was tested using cell clone formation assay. The effect of Polyphyllin I on cell cycle and apoptosis were confirmed by flow cytometry and TUNEL assay. Western blot was used to test the effect of Polyphyllin I on JAK/STAT3 pathway and apoptosis related proteins. The subcutaneous GC mouse model was established to examine whether polyphyllin I could inhibit GC growth in vivo. Results: A dual-luciferase reporter assay showed that polyphyllin I could inhibit the activity of Bcl-2 which is downstream of JAK2/STA3. Polyphyllin I significantly inhibited GC cell proliferation and induced cell apoptosis in a dose-dependent manner. The western blot results indicated that polyphyllin I mainly inhibited the phosphorylation of STAT3 by the way which is different from AG490. It was inferred that polyphyllin I may inhibit the JAK2/STAT3 pathway and affect the expression level of apoptosis related genes. Finally, in the tumor xenograft experiment proved that polyphyllin I significantly inhibited the growth of GC in vivo.Conclusions: Polyphyllin I may play its anticancer activity by inhibiting phosphorylation of STAT3 in GC cells.