From mechanism to clinical: research evolution and hotspot analysis of CD276/B7-H3 in cancer immunotherapy

Background CD276 (B7-H3) is a pivotal immune checkpoint molecule with dual roles in T-cell regulation and tumor immune evasion, representing a promising therapeutic target across multiple cancers. However, a comprehensive analysis of the research landscape, evolutionary pathways, and knowledge structure in this field remains lacking. Methods Publications related to CD276/B7-H3 in cancer research were systematically retrieved from the Web of Science Core Collection (WoS, n = 688) and Scopus (n = 759) spanning from January 2001 to August 2025. After merging and de-duplication, a final corpus of 830 publications was analyzed using Bibliometrix, VOSviewer, CiteSpace, and Pajek to evaluate publication trends, influential authors and institutions, collaboration networks, core journals, co-citation patterns, and keyword evolution. Results The field exhibited exponential growth with an annual publication increase of 21.77%. China and the United States were the dominant contributing countries. Journal for Immunotherapy of Cancer was the most productive journal, while Clinical Cancer Research produced the most impactful publications. Co-citation analysis highlighted foundational studies on B7-H3’s prognostic significance and recent breakthroughs in CAR T-cell therapy targeting B7-H3. Keyword evolution revealed a clear transition from early themes such as “expression” and “prognosis” to contemporary focuses including “immunotherapy,” “tumor microenvironment,” and “chimeric antigen receptor”. Conclusion This study provides the first integrated bibliometric overview of CD276/B7-H3 research in cancer, illustrating a rapid transition from mechanistic exploration to clinical application. The findings underscore B7-H3’s importance as a pan-cancer antigen and immunotherapeutic target, offering valuable insights for guiding future research directions.