This review discusses the molecular mechanisms and therapeutic potential of apigenin, a flavonoid, in combating cancer metastasis. Apigenin has been shown to modulate key signaling pathways involved in cancer cell proliferation, invasion, and metastasis, including JAK/STAT, PI3K/Akt/mTOR, MAPK/ERK, NF-κB, and Wnt/β-catenin pathways, as well as oncogenic non-coding RNA networks. The review highlights apigenin's ability to target these pathways to suppress cancer proliferation, specifically focusing on its effects on angiogenesis, epithelial-to-mesenchymal transition (EMT), maintenance of cancer stem cells (CSCs), cell cycle arrest, and cancer cell death. Apigenin's anti-angiogenic effects are attributed to its ability to inhibit HIF-1α activity and disrupt the HIF-1/VEGF axis. In EMT, apigenin inhibits the expression of E-cadherin and promotes the expression of mesenchymal markers like N-cadherin and vimentin, thereby suppressing tumor growth and invasion. Apigenin also inhibits CSCs by targeting multiple signaling pathways and transcription factors, such as YAP/TAZ, CK2, and p53. Additionally, apigenin arrests the cell cycle at both G2/M and G1/S checkpoints, leading to cell cycle arrest and apoptosis. The review also explores how apigenin induces various forms of programmed cell death, including apoptosis, autophagy, ferroptosis, necroptosis, and anoikis, depending on the tumor type and cell properties. Overall, the review emphasizes the multifaceted role of apigenin in cancer management and its potential as a therapeutic agent against cancer metastasis.This review discusses the molecular mechanisms and therapeutic potential of apigenin, a flavonoid, in combating cancer metastasis. Apigenin has been shown to modulate key signaling pathways involved in cancer cell proliferation, invasion, and metastasis, including JAK/STAT, PI3K/Akt/mTOR, MAPK/ERK, NF-κB, and Wnt/β-catenin pathways, as well as oncogenic non-coding RNA networks. The review highlights apigenin's ability to target these pathways to suppress cancer proliferation, specifically focusing on its effects on angiogenesis, epithelial-to-mesenchymal transition (EMT), maintenance of cancer stem cells (CSCs), cell cycle arrest, and cancer cell death. Apigenin's anti-angiogenic effects are attributed to its ability to inhibit HIF-1α activity and disrupt the HIF-1/VEGF axis. In EMT, apigenin inhibits the expression of E-cadherin and promotes the expression of mesenchymal markers like N-cadherin and vimentin, thereby suppressing tumor growth and invasion. Apigenin also inhibits CSCs by targeting multiple signaling pathways and transcription factors, such as YAP/TAZ, CK2, and p53. Additionally, apigenin arrests the cell cycle at both G2/M and G1/S checkpoints, leading to cell cycle arrest and apoptosis. The review also explores how apigenin induces various forms of programmed cell death, including apoptosis, autophagy, ferroptosis, necroptosis, and anoikis, depending on the tumor type and cell properties. Overall, the review emphasizes the multifaceted role of apigenin in cancer management and its potential as a therapeutic agent against cancer metastasis.