BackgroundIncreasing evidence suggests that microRNAs (miRNAs) play critical roles in malignant transformation, tumor progression and metastasis. Aberrant miR-655-3p expression has been associated with several cancers. However, the role and underlying mechanism of miR-655-3p in the development of hepatocellular carcinoma (HCC) remains unclear.MethodsMiR-655-3p expression was detected by quantitative RT-PCR (qRT-PCR) in human HCC tissues and cell lines. Cell proliferation was investigated using MTT and colony formation assays, and cell migration and invasion abilities were evaluated by transwell assay. ADAM10 protein expression was detected by immunohistochemical assay. The target gene and downstream of miR-655-3p were determined by qRT-PCR, western blot and dual-luciferase reporter assays.ResultsmiR-655-3p was significantly down-regulated in HCC tissues and HCC cell lines. Low miR-655-3p expression was negatively related to tumor size, portal vein tumor thrombosis (PVTT) status, TNM stage and metastasis status. In addition, miR-655-3p overexpression and depletion decreased and increased HCC cell proliferation, migration and invasion, respectively. Moreover, ADAM10 was identified as a direct target of miR-655-3p, and miR-655-3p down-regulated E-cadherin protein level and inhibits β-catenin pathway by mediating ADAM10.ConclusionsMiR-655-3p might functions as a tumor suppressor by directly targeting ADAM10 and indirectly regulating β-catenin pathway in the development of progression of HCC. It may be a novel therapeutic candidate target to in HCC treatment.

BackgroundRecent studies have shown that miR-372 plays important roles in hepatocellular carcinoma (HCC) progression. However, results have been conflicting regarding its expression levels and role in HCC.MethodsRT-PCR and in situ hybridization was used to evaluate miR-372 expression in HCC tissues and cell lines. The methylation status of neighboring CpG islands upstream of the miR-372 promoter was analyzed by methylation-specific PCR (MSP). Transfection of miR-372 mimic into HCC cell lines was used to evaluate cellular proliferation and invasion. Prognostic significance was analyzed by the Kaplan–Meier survival method and Cox regression.ResultsmiR-372 was expressed at lower levels in HCC tissues compared with controls and was related to tumor metastasis and poor prognosis. Hypermethylation of miR-372 was detected in HCC cell lines and tissues, and miR-372 expression was restored upon 5-aza-dCyd treatment. Upregulated expression by mir-372 mimic transfection inhibited proliferation and invasion capacity in HCC cells.ConclusionsmiR-372 may play an important role in hepatic carcinogenesis and may serve as a new target or method to detect and treat HCC in the future.

With the development of laparoscopy and digestive endoscopy, multiple laparoscopic and endoscopic cooperative surgeries (LECSs) for gastrointestinal stromal tumors have recently been developed. Classic LECS has been confirmed as a feasible and safe treatment procedure for gastrointestinal stromal tumors with regard to both short-term surgical and long-term oncological outcomes; however, classic LECS has the potential risk of gastric contents or tumor cells spilling into the abdominal cavity because the gastric wall has to be opened during the procedure. Various modified LECS techniques have aimed at further minimizing invasiveness, such as the full-thickness resection method using the nonexposure technique (combination of laparoscopic and endoscopic approaches to neoplasia with a nonexposure technique), nonexposed endoscopic wall­inversion surgery, and closed LECS. This review describes and summarizes the current LECS for gastrointestinal tumor.