RESUMO
Objective To understand the relationship between air pollutants and digestive system cancers, and to provide a reference for future research and prevention and control of digestive system cancer. Methods All relevant literature published in English between 1970-2022 was searched through the databases of PubMed, web of science and Embase, and meta-analysis was used to explore the effects of specific air pollutants on digestive system cancers. Results PM2.5 was able to increase the risk of incidence or mortality of total digestive cancers by 11% (1.05 to 1.17). For specific cancers, PM2.5 was only associated with an increased risk of liver cancer in this study, with a combined RR (95% CI) of 1.31 (1.19 to 1.46), while there was no statistically significant association with other specific digestive cancers ( P>0.05）. NO2 increased the risk of incidence or mortality of total digestive cancers by 3% (1.00 to 1.07). Conclusion For specific digestive system cancers, PM2.5 has the most pronounced effect on liver cancer. More evidence is needed to support the relationship between NO2 and cancer. Currently, it has been observed that NO2 has a negative effect on overall digestive cancers. This study provides insights for the prevention and control of digestive system cancer in countries and regions with high PM2.5 and NO2 concentrations.
RESUMO
Digestive system cancers, including liver, gastric, colon, esophageal and pancreatic cancers, are the leading cause of cancers with high morbidity and mortality, and the question of their clinical treatment is still open. Previous studies have indicated that Ziyuglycoside II (ZYG II), the major bioactive ingredient extract from Sanguisorba officinalis L., significantly inhibits the growth of various cancer cells. However, the selective anti-tumor effects of ZYG II against digestive system cancers are not systemically investigated. In this study, we reported the anti-cancer effect of ZYG II on esophageal cancer cells (OE21), cholangiocarcinoma cells (HuCCT1), gastric cancer cells (BGC-823), liver cancer cells (HepG2), human colonic cancer cells (HCT116), and pancreatic cancer cells (PANC-1). We also found that ZYG II induced cell cycle arrest, oxidative stress and mitochondrial apoptosis. Network pharmacology analysis suggested that UBC, EGFR and IKBKG are predicted targets of ZYG II. EGFR signaling was suggested as the critical pathway underlying the anti-cancer effects of ZYG II and both docking simulation and western blot analysis demonstrated that ZYG II was a potential EGFR inhibitor. Furthermore, our results showed synergistic inhibitory effects of ZYG II and chemotherapy 5-FU on the growth of cancer cells. In summary, ZYG II are effective anti-tumor agents against digestive cancers. Further systemic evaluation of the anti-cancer activities in vitro and in vivo and characterization of underlying mechanism will promote the development of novel supplementary therapeutic strategies based on ZYG II for the treatment of digestive system cancers.