Prophylactic stenting for esophageal stricture prevention after endoscopic submucosal dissection

Endoscopic submucosal dissection (ESD) of superficial esophageal cancer has been increasingly used as an alternative to surgery because it is minimally invasiveand has a high rate of en bloc resection. However, a high rate of esophageal stricture is observed after ESD for large lesions, which can dramatically decrease the patient's quality of life. Stricture prevention is necessary to allow for endoscopic therapy to expand. We, herein, review the most recent evidence and discuss the role of the metallic self-expandable stent and the biodegradable stent in esophageal stricture prevention. Limited studies suggested that prophylactic stenting could reduce the stricture rate without increasing the number of complications. In addition, the number of bougie dilation procedures was significantly lower with stent placement. Esophageal stenting is a promising option for post-ESD stricture prevention. However, current evidence is too preliminary to formulate practice standards. Future studies are needed to further validate the efficacy and safety of prophylactic stenting and determine the best strategy for stricture prevention. Stent migration is the most common complication. A new stent that has advantages of a low migration rate and minimal tissue reaction will need to be developed. Therefore, randomized controlled trials with long-term follow-up periods are required before prophylactic stenting could be considered a valid option to prevent post-ESD stricture.

Blockage of ETS homologous factor inhibits the proliferation and invasion of gastric cancer cells through the c-Met pathway

BACKGROUND Gastric cancer(GC)is one of the most common and deadliest types of cancer worldwide due to its delayed diagnosis and high metastatic frequency,but its exact pathogenesis has not been fully elucidated.ETS homologous factor(EHF)is an important member of the ETS family and contributes to the pathogenesis of multiple malignant tumors.To date,whether EHF participates in the development of GC via the c-Met signaling pathway remains unclear.AIM To investigate the role and mechanism of EHF in the occurrence and development of GC.METHODS The expression of EHF mRNA in GC tissues and cell lines was measured by quantitative PCR.Western blotting was performed to determine the protein expression of EHF,c-Met,and its downstream signal molecules.The EHF expression in GC tissues was further detected by immunohistochemical staining.To investigate the role of EHF in GC oncogenesis,small interfering RNA(siRNA)against EHF was transfected into GC cells.The cell proliferation of GC cells was determined by Cell Counting Kit-8 and colony formation assays.Flow cytometry was performed following Annexin V/propidium iodide(PI)to identify apoptotic cells and PI staining to analyze the cell cycle.Cell migration and invasion were assessed by transwell assays.RESULTS The data showed that EHF was upregulated in GC tissues and cell lines in which increased expression of c-Met was also observed.Silencing of EHF by siRNA reduced the proliferation of GC cells.Inhibition of EHF induced significant apoptosis and cell cycle arrest in GC cells.Cell migration and invasion were significantly inhibited.EHF silencing led to c-Met downregulation and further blocked the Ras/c-Raf/extracellular signal-related kinase 1/2(Erk1/2)pathway.Additionally,phosphatase and tensin homolog was upregulated and glycogen synthase kinase 3 beta was deactivated.Moreover,inactivation of signal transducer and activator of transcription 3 was detected following EHF inhibition,leading to inhibition of the epithelial-to-mesenchymal transition(EMT).CONCLUSION These results suggest that EHF plays a key role in cell proliferation,invasion,apoptosis,the cell cycle and EMT via the c-Met pathway.Therefore,EHF may serve as an antineoplastic target for the diagnosis and treatment of GC.