Systematic review synthesizes preclinical evidence on luteolin's anticancer effects in gastric cancer, highlighting its mechanisms.
Purpose Luteolin, a naturally occurring dietary flavonoid, has attracted increasing attention as a potential therapeutic and chemosensitizing agent in gastric cancer. This study aims to synthesize and critically evaluate the available preclinical evidence on the anticancer effects and underlying cellular and molecular mechanisms of luteolin in gastric cancer. Design/methodology/approach A comprehensive systematic search of PubMed, Embase, Web of Science, Scopus and Google Scholar was conducted to identify relevant studies published up to December 31, 2025. Eligible preclinical studies, in vitro and in vivo, investigating the effects of luteolin on gastric cancer models were included. Study selection and data extraction were performed in accordance with PRISMA guidelines, and the findings were narratively synthesized. Findings A total of 27 preclinical studies met the inclusion criteria. Across the included in vitro studies, luteolin consistently reduced gastric cancer cell viability and proliferation, induced apoptosis and caused cell-cycle arrest at the G0/G1 and/or G2/M phases. Luteolin suppressed migration and invasion, decreased epithelial–mesenchymal transition markers and modulated oxidative stress and inflammatory mediators. In vivo, luteolin inhibited tumor growth, reduced metastatic burden without overt toxicity and enhanced the chemosensitivity of gastric tumors to conventional agents in combination settings. Originality/value The available evidence from preclinical in vitro and in vivo models supports the anticancer potential of luteolin in gastric cancer and highlights its capacity to modulate multiple cellular and molecular targets. Nonetheless, these findings are derived exclusively from preclinical studies, and well-designed clinical trials are required before any definitive therapeutic conclusions can be drawn.
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Mar’ie et al. (2026) studied this question.
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