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.

A Tool for the Treatment of Gastrointestinal Tumors: Micro- Ecological Immunotherapy

It has been proposed that the intestinal microbiota and gastrointestinal tumors are interdependent.Changes in the microbiota can cause dysfunction of the gastrointestinal tract,thereby promoting carcinogenic changes,leading to the occurrence of gastrointestinal tumors.Recent studies on intestinal microbiota have opened up a new area in intestinal micro-ecological immunotherapy.The intestinal microbiota is a double-edged sword.Gut microbes participate in carcinogenesis,but can also be used for immunotherapy.The intestinal microbiota is also regulated by the daily diet.Intestinal micro-ecological immunotherapy combines intestinal immune nutrition and intestinal ecological nutrition to make full use of the intestinal microbiota to strengthen nutritional support.Micro-ecological immunotherapy enhances the body’s immune function by providing energy,improving the functional state of tissues and organs,protecting the intestinal mucosal barrier and maintaining normal intestinal microbiota balance.This involves,to some extent,PD-1 and PD-L1.The microbiota is beneficial to improve the clinical efficacy of conventional anti-cancer therapy and to reduce the incidence of complications.At the same time,micro-ecological immunotherapy is itself active and effective in the perioperative treatment of tumors,which is of great significance for the prognosis of the patient.Gastrointestinal tumors are increasingly linked to intestinal microbiota,and various microbiota-related technologies and drugs have been developed.In the future,the intestinal microbiota may represent a screening marker for gastrointestinal tumors.In addition,clinicians may be able to prevent and treat cancers by changing the gene expression levels of certain microbiota,or by regulating the types of microbes present.

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.