Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors in the gastrointestinal tract, and about 60% of them are found in the stomach. With the widespread application of endoscopy and endoscopic ultrasonography (EUS), more and more gastric GISTs are being found in an early stage (with a relative small diameter and no metastasis), giving the chance of complete resection. Endoscopic resection such as endoscopic band ligation (EBL), endoscopic submucosal dissection (ESD), endoscopic submucosal excavation (ESE), endoscopic full-thickness resection (EFTR) and submucosal tunneling endoscopic resection (STER), is a minimally invasive method compared with the conventional surgical approaches (open or laparoscopic), and has been demonstrated to be safe and effective for treating gastric GISTs. This review summarizes the recent advances on endoscopic resection of gastric GISTs, aiming to provide a rational management strategy for gastric GISTs.

Purpose: To investigate the expression of histone deacetylase 6 (HDAC6) in colon cancer and its role in colon cancer cell growth and migration. Materials and methods: We detected the expression of HDAC6 in a colon cancer tissue chip using immunochemical staining, and analyzed the difference in HDAC6 expression between cancer and adjacent noncancerous tissues. Then, we explored the relationship between HDAC6 expression and patients’ clinicopathological characteristics and prognoses. In adidition, the role of HDAC6 in colon cancer cell growth and migration, as well as its potential related signal pathway, through HDAC6 knockdown was explored. Results: The immunochemical score of HDAC6 expression was higher in cancer tissue than in the adjacent noncancerous tissue (4.54 vs 3.08, P<0.005); similarly, as well as the rate of high HDAC6 expression was higher in cancer tissue than in the adjacent noncancerous tissue (71.1% vs 40.9%, P<0.001). Patients showing high HDAC6 expression had a shorter overall survival time. Additionally, Cox regression analysis showed that high HDAC6 expression was an independent risk factor for poor prognosis. HDAC6 knockdown decreased cell viability, colony formation, and number of migrated colon cancer cells (HCT116 and HT29); the expression of p-MEK, p-ERK, and p-AKT was also decreased, but had no influence on MEK, ERK, and AKT expression. Conclusion: HDAC6 is highly expressed in colon cancer and associated with a poor prognosis. HDAC6 knockdown inhibits colon cancer cell growth and migration, partly through the MAPK/ERK pathway.

The extracellular matrix (ECM) provides physical support and imparts significant biochemical and mechanical cues to cells. Matrix stiffening is a hallmark of liver fibrosis and is associated with many hepatic diseases, especially liver cirrhosis and carcinoma. Increased matrix stiffness is not only a consequence of liver fibrosis but is also recognized as an active driver in the progression of fibrotic hepatic disease. In this article, we provide a comprehensive view of the role of matrix stiffness in the pathological progression of hepatic disease. The regulators that modulate matrix stiffness including ECM components, MMPs, and crosslinking modifications are discussed. The latest advances of the research on the matrix mechanics in regulating intercellular signaling and cell phenotype are classified, especially for hepatic stellate cells, hepatocytes, and immunocytes. The molecular mechanism that sensing and transducing mechanical signaling is highlighted. The current progress of ECM stiffness’s role in hepatic cirrhosis and liver cancer is introduced and summarized. Finally, the recent trials targeting ECM stiffness for the treatment of liver disease are detailed.

Endoscopic submucosal dissection (ESD) has been widely applied as a less invasive and more effective method for treating early esophageal cancers such as squamous cell carcinoma and dysplasia of Barrett’s esophagus. However, post-ESD esophageal stricture often occurs if patients suffer circumferential mucosal defects of more than three-quarters of the circumference of the esophagus, which makes it difficult for patients to swallow and greatly reduces their quality of life. Moreover, there is currently no standard method to treat post-ESD esophageal stricture, even though it is extraordinarily important to prevent its formation. In recent years, several strategies to prevent esophageal stricture have emerged. These strategies can be classified into pharmacological, mechanical, tissue engineering, and other novel strategies, with each strategy having its own strengths and weaknesses. Although the pharmacological prophylaxis and mechanical strategies are relatively mature, they still have their drawbacks like high time-consumption, the occurrence of re-stricture, and significant side effects. Tissue engineering strategies and other novel strategies have shown promising preliminary results, but more clinical trials are needed. In this review, we discuss these strategies, with a particular focus on tissue engineering strategies and other novel strategies. It is hoped that this discussion will aid in finding more effective and safer strategies to prevent esophageal stricture.

The deacetylation process regulated by histone deacetylases (HDACs) plays an important role in human health and diseases. HDAC6 belongs to the Class IIb of HDACs family, which mainly modifies non-histone proteins located in the cytoplasm. HDAC6 plays a key role in tumors, neurological diseases, and inflammatory diseases. Therefore, targeting HDAC6 has become a promising treatment strategy in recent years. ACY-1215 is the first orally available highly selective HDAC6 inhibitor, and its efficacy and therapeutic effects are being continuously verified. This review summarizes the research progress of ACY-1215 in cancer and other human diseases, as well as the underlying mechanism, in order to guide the future clinical trials of ACY-1215 and more in-depth mechanism researches.

Background: ACY1215 is a selective histone deacetylase 6 (HDAC6) inhibitor, and can suppress tumor growth for many human cancers. However, its role in colon cancer and its impact on the chemotherapeutic effect of 5-fluorouracil (5-Fu) are largely unknown. The aim of the present study is to explore the effect of ACY1215 on cell growth, migration, invasion and apoptosis, along with its impact on the chemotherapeutic effect of 5-Fu in HCT116 cells. Methods: HCT116 cells were treated with ACY1215 with or without 5-Fu, and cell viability, proliferation, migration, invasion and apoptosis were explored. Results: The cell viability, colony formation number, wound closure rate, and migrated cell numbers of HCT116 cells significantly decreased, while the apoptotic cells significantly increased with the increased concentration of ACY1215 (P<0.05). The combination of ACY1215 and 5-Fu was more potent than either drug alone, as indicated by an increase of apoptotic cells, and by a decrease of cell viability, colony formation number, wound closure rate and migrated cell numbers. The expression of phosphorylated mitogen-activated protein kinases (pMEK) and phosphorylated extracellular-signal regulated protein kinase (pERK) were decreased when HCT116 cells were cultured with ACY1215. Conclusions: Selective HDAC6 inhibitor, ACY1215, could inhibit the cell proliferation, migration and invasion, and induce apoptosis of HCT116 colon cancer cells. Furthermore, ACY1215 may enhance the chemotherapeutic effect of 5-Fu in HCT116 cells.