Abstract
Simple SummaryMicrobial dysbiosis has been credited as one of the contributing factors to the development and progression of gastrointestinal tract cancer. The altered microbiota influences carcinogenesis through the induction of instability and damage to genetic material, modulation of host metabolic and inflammatory pathways, production of carcinogenic metabolites, and suppression of host antitumor response. These microbes secrete extracellular vesicles that are possibly carrying carcinogenic bioactive metabolites within their cargo. Studies have illustrated the ability of bacterial extracellular vesicles to cross the intestinal epithelial barrier and selectively accumulate near intestinal tumor cells. The purpose of this systemic review was to highlight the possible role of gut bacterial vesicles in the development, progression, and pathogenesis of gastrointestinal tract cancer and their possible involvement in the modulation of the tumor microenvironment. An infinitesimal amount of research has been carried out on the impact of bacterial extracellular vesicles on oncogenesis and tumor progression. This review aimed to encourage more investigations on this subject.Bacterial extracellular vesicles are membrane-enclosed, lipid bi-layer nanostructures that carry different classes of biomolecules, such as nucleic acids, lipids, proteins, and diverse types of small molecular metabolites, as their cargo. Almost all of the bacteria in the gut secrete extracellular vesicles to assist them in competition, survival, material exchange, host immune modulation, infection, and invasion. The role of gut microbiota in the development, progression, and pathogenesis of gastrointestinal tract (GIT) cancer has been well documented. However, the possible involvement of bacterial extracellular vesicles (bEVs) in GIT cancer pathophysiology has not been given due attention. Studies have illustrated the ability of bEVs to cross physiological barriers, selectively accumulate near tumor cells, and possibly alter the tumor microenvironment (TME). A systematic search of original published works related to bacterial extracellular vesicles on gastrointestinal cancer was performed for this review. The current systemic review outlines the possible impact of gut microbiota derived bEVs in GIT cancer in light of present-day understanding. The necessity of using advanced sequencing technologies, such as genetic, proteomic, and metabolomic investigation methodologies, to facilitate an understanding of the interrelationship between cancer-associated bacterial vesicles and gastrointestinal cancer is also emphasized. We further discuss the clinical and pharmaceutical potential of bEVs, along with future efforts needed to understand the mechanism of interaction of bEVs in GIT cancer pathogenesis.
Highlights
The human gastrointestinal system is one of the most complex known microbial systems; it is colonized by trillions of microorganisms, including bacteria, archaea, fungi, and viruses [1,2], with bacteria being the largest group [3]
Alterations in microbial community in gastrointestinal tract (GIT) may lead to a loss of ability to maintain homeostatic conditions, which contributes to cancer pathogenesis and progression [9,10]
Substantial evidence indicates that the carcinogenic effects of microbiota can be transferred to healthy mice by fecal microbiota transfer (FMT) from mice or human patients suffering from GIT cancer [13]
Summary
The human gastrointestinal system is one of the most complex known microbial systems; it is colonized by trillions of microorganisms, including bacteria, archaea, fungi, and viruses [1,2], with bacteria being the largest group [3]. Studies have indicated that microbiota influence the development and progression of cancer by modulating the tumor microenvironment (TME) [4,5,6,7]. Alterations in microbial community in GIT may lead to a loss of ability to maintain homeostatic conditions, which contributes to cancer pathogenesis and progression [9,10]. Studies suggest that dysbiosis of the gut microbiome alters its metabolic products, influencing host metabolic and inflammatory pathways, thereby disturbing homeostasis and paving the way to carcinogenesis [11]. Microbial dysbiosis has been attributed to reduced responses to anticancer therapies due to the ability of certain microbes to metabolize drugs and influence immune responses within the TME [12]. Substantial evidence indicates that the carcinogenic effects of microbiota can be transferred to healthy mice by fecal microbiota transfer (FMT) from mice or human patients suffering from GIT cancer [13]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
