Gastric cancer (GC) is a common malignancy and a major cause of cancer mortality worldwide. While Helicobacter pylori is well-known as a key factor in GC development, recent evidence highlights the role of gastric microbiota in disease progression. Dysregulation of gastric microbiota plays a critical role in GC development, from precancerous lesions to malignancy. This review summarizes current understanding of gastric microbiota in GC development and evaluates the potential clinical applications of gastric microbes for diagnosis, prognosis, and treatment. It also discusses current conceptual challenges and limitations. Modulating gastric microbiota is a promising approach for GC prevention and management, requiring further research. The gastric microbiota is influenced by factors such as acid suppression, medication use, and carcinogenic processes. Gastric microbial dysbiosis is associated with GC, with altered microbial diversity and richness observed in gastric tissues, oral, and faecal samples of GC patients. Pathogenic microbes such as Streptococcus anginosus and Fusobacterium are enriched in GC tumour tissues and may promote tumourigenesis. Other pathogenic bacteria, including F. nucleatum and Propionibacterium acnes, also contribute to GC development. Pathogenic fungi and viruses, such as Candida and Epstein-Barr virus, are also involved in GC. Beneficial microbes, such as Bifidobacterium and Lactobacillus, may inhibit GC by modulating the immune system and reducing inflammation. Probiotics can help restore gastric microbiota after H. pylori eradication and may enhance the effectiveness of GC treatment. Microbial biomarkers show promise for GC diagnosis and prognosis, with some showing high accuracy in distinguishing GC from non-malignant lesions. However, challenges remain in translating these findings into clinical practice. The interaction between H. pylori and non-H. pylori microbes is complex, with H. pylori infection leading to gastric dysbiosis that can be reversed by eradication. However, non-H. pylori pathobionts may still contribute to GC development. Probiotics can inhibit H. pylori and reduce its harmful effects. The therapeutic potential of gastric microbiota is being explored, with strategies such as probiotics, prebiotics, and faecal microbiota transplantation showing promise. However, the mechanisms by which gastric microbes affect treatment outcomes remain unclear. Future research should focus on understanding the role of gastric microbiota in GC, including its interactions with host cells and the impact of microbial metabolites on cancer progression. Standardized methodologies and large-scale studies are needed to clarify the dynamic microbial landscape in GC. The development of microbiota-based strategies for GC prevention and treatment is a promising frontier, requiring further investigation.Gastric cancer (GC) is a common malignancy and a major cause of cancer mortality worldwide. While Helicobacter pylori is well-known as a key factor in GC development, recent evidence highlights the role of gastric microbiota in disease progression. Dysregulation of gastric microbiota plays a critical role in GC development, from precancerous lesions to malignancy. This review summarizes current understanding of gastric microbiota in GC development and evaluates the potential clinical applications of gastric microbes for diagnosis, prognosis, and treatment. It also discusses current conceptual challenges and limitations. Modulating gastric microbiota is a promising approach for GC prevention and management, requiring further research. The gastric microbiota is influenced by factors such as acid suppression, medication use, and carcinogenic processes. Gastric microbial dysbiosis is associated with GC, with altered microbial diversity and richness observed in gastric tissues, oral, and faecal samples of GC patients. Pathogenic microbes such as Streptococcus anginosus and Fusobacterium are enriched in GC tumour tissues and may promote tumourigenesis. Other pathogenic bacteria, including F. nucleatum and Propionibacterium acnes, also contribute to GC development. Pathogenic fungi and viruses, such as Candida and Epstein-Barr virus, are also involved in GC. Beneficial microbes, such as Bifidobacterium and Lactobacillus, may inhibit GC by modulating the immune system and reducing inflammation. Probiotics can help restore gastric microbiota after H. pylori eradication and may enhance the effectiveness of GC treatment. Microbial biomarkers show promise for GC diagnosis and prognosis, with some showing high accuracy in distinguishing GC from non-malignant lesions. However, challenges remain in translating these findings into clinical practice. The interaction between H. pylori and non-H. pylori microbes is complex, with H. pylori infection leading to gastric dysbiosis that can be reversed by eradication. However, non-H. pylori pathobionts may still contribute to GC development. Probiotics can inhibit H. pylori and reduce its harmful effects. The therapeutic potential of gastric microbiota is being explored, with strategies such as probiotics, prebiotics, and faecal microbiota transplantation showing promise. However, the mechanisms by which gastric microbes affect treatment outcomes remain unclear. Future research should focus on understanding the role of gastric microbiota in GC, including its interactions with host cells and the impact of microbial metabolites on cancer progression. Standardized methodologies and large-scale studies are needed to clarify the dynamic microbial landscape in GC. The development of microbiota-based strategies for GC prevention and treatment is a promising frontier, requiring further investigation.