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In this review, we outline the new expertise and research progress with luteolin as an antitumor agent, and clarify the related results from the aspects of tumor proliferation, apoptosis, invasion, metastasis, sensitivity to radiotherapy and chemotherapy, angiogenesis, and immunotherapy. In recent years, with the development of medical technology, the early detection rate of tumors has increased significantly. However, the number of cancer patients remains high. Therefore, a new and reasonably effective tumor therapeutic drug is urgently demanded. Luteolin, a flavonoid and widespread in nature, attracts more and more attention due to its universal biological utility, especially in the study of antitumor activity. This article reviews the work published in the past 20 years on the role and mechanism of luteolin as an antitumor agent, showing that this compound has a variety of effects for antitumor treatment by acting on different cytokines. Although clinical studies have not yet been widely carried out, a series of basic studies have confirmed that luteolin is a reasonably effective antineoplastic agent or anticancer adjuvant. Besides, derivatives of luteolin have good application prospects.

Purpose: The high mortality rate of malignant tumors is often attributable to the loss of surgical opportunities due to late diagnosis when invasion and metastasis have significantly affected the patient. A hypoxic microenvironment can promote the progression of malignant tumors. This study explored the invasion resistance and migration ability of luteolin-Zn complexes. Methods: We created a low-oxygen environment using a 3-atmosphere incubator. The appropriate drug concentration was determined using the CCK8 experiment. We determined its role in cell invasion and migration through scratch and transwell experiments. Western blotting, polymerase chain reaction, and cellular immunity experiments were used to study the mechanism and its impact on the secretion of invasion and migration factors. Results: Our results indicated that the luteolin-Zn complex significantly reduced MMP2, MMP9, N-Ca, and HIF-1ɑ expression. It also upregulated TIMP1 and E-Ca expression. Moreover, its capabilities may be achieved by regulating the AMPK/mTOR and PI3K/Akt/mTOR signaling pathways. Conclusions: The luteolin-Zn complex was highly resistant to the invasion and migration of M2-like tumor-related macrophages. This may exert a unique influence on mTOR by integrating various signals. This study suggests that the luteolin-Zn complex has a strong anticancer effect under hypoxic conditions.