The Mechanism of CagA and VacA in Gastric Cancer under the Tumor Microenvironment and Vitro Factors

Gastric cancer is closely related to the stomach microbiota,especially Helicobacter pylori.Numerous reports and clinical studies have shown that microbial behavior in the stomach may lead to pathological changes in the gastrointestinal tract of the host,which ultimately leads to the production and development of gastric cancer.This review outlines the major pathogenic processes of Helicobacter pylori in the stomach,specifically focusing on Cag A,Vac A,inflammatory pathways and oxidative stress.In addition,we describe the effects of some non-Helicobacter pylori factors,such as other microbiota,alcohol,and tobacco,on the carcinogenesis induced by Helicobacter pylori.The effects of family history are also taken into account.We hope that understanding the stomach microbiota will make it possible to more easily prevent,detect and treat gastric cancer.

Microbiota:a Sword that Breaks Through Diabetes

Diabetes are a group of metabolic disorders characterized by persistent hyperglycemia that is a major public health problem.Middle-aged and elderly people are at the highest risk of type 2 diabetes,but younger cases are now being diagnosed with greater frequency.Numerous clinical studies have reported that the behavior of the intestinal microbiota may affect the development of metabolic disorders in humans,including obesity and diabetes.This review describes the relationship between the gut microbiota and diabetes,and discusses the possible mechanisms underlying their involvement in the development of type 1 diabetes,obesity,and type 2 diabetes.By better understanding the intestinal microbiota,it may become possible to treat diabetes and obesity by manipulating the gut microbes through probiotics and dietary changes,fecal microbiota transplantation,or surgical approaches.

PSC-induced Galectin-1 Promotes the Malignant Behavior of Pancreatic Ductal Adenocarcinoma

Background Galectin-1 is aβ-galactoside-binding protein overexpressed in the pancreatic stellate cells(PSCs)of pancreatic ductal adenocarcinoma(PDAC),while its expression is typically low in pancreatic cancer cells(PCCs).The point at which galectin-1 expression in PCCs increases,and its association with PDAC progression,have been unclear.Methods Galectin-1 expression in PDAC and metastatic lymph nodes was investigated using an immunohistochemical assay.PANC-1 PCC cells were co-cultured with PSCs expressing different levels of galectin-1.Subsequently,galectin-1 was overexpressed in PANC-1 cells using recombinant lentiviruses,and their proliferation,invasion,anchorage-independent growth,and in vivo tumorigenicity were evaluated.Results There was intermediate galectin-1 expression in PCCs,and it was positively associated with galectin-1 expression in PSCs in the PDAC tissues.Galectin-1 was strongly expressed in the metastatic lymph nodes.In the co-culture,high galectin-1 expression in the PSCs increased the galectin-1 expression in the PANC-1 cells.The galectin-1 overexpression in the PANC-1 cells enhanced their clone formation ability,proliferation,and invasion,increased the expression of proliferating cell nuclear antigen(PCNA)and BCL-2,and decreased Bax expression,promoting the establishment and growth of tumors.Conclusion High galectin-1 expression in PSCs induces galectin-1 expression in PCCs and subsequently promotes the malignant biological behavior of PDAC.