4.6 Review

Luteolin, a Potent Anticancer Compound: From Chemistry to Cellular Interactions and Synergetic Perspectives

Journal

CANCERS
Volume 14, Issue 21, Pages -

Publisher

MDPI
DOI: 10.3390/cancers14215373

Keywords

luteolin; apoptosis and cell cycle; anti-metastasis; anti-inflammation; synergistic action

Categories

Funding

  1. Jazan University, Saudi Arabia
  2. ICMR-DHR, Young Scientist Fellowship [R. 12014/29/2022/HR]

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Luteolin, a common flavonoid, has shown promising anticancer properties by targeting various cellular processes to inhibit tumor growth and reverse medication resistance in cancer cells.
Simple Summary Common flavonoid luteolin 3 ',4 ',5,7-tetrahydroxyflavone has immense potential to be utilized as a chemopreventive dietary molecule. According to available data, luteolin interacts with a number of known cellular targets and prevents the growth of cancer cells by triggering apoptosis and cell cycle arrest. Inhibiting tumor cell metastasis and angiogenesis is another promising function of luteolin, according to recent research. Luteolin has also been discovered to be a good option for synergistic investigations and may be able to reverse cancer cells' medication resistance. The current review focuses on the work being done to find molecular targets of luteolin in cancer. Additionally, the use of luteolin combinations and delivery systems enabled by nanotechnology are presented. The review is distinctive by offering all potential cellular targets of luteolin in cancer on one platform. The text is accompanied by excellent visual aids. Increasing rates of cancer incidence and the toxicity concerns of existing chemotherapeutic agents have intensified the research to explore more alternative routes to combat tumor. Luteolin, a flavone found in numerous fruits, vegetables, and herbs, has exhibited a number of biological activities, such as anticancer and anti-inflammatory. Luteolin inhibits tumor growth by targeting cellular processes such as apoptosis, cell-cycle progression, angiogenesis and migration. Mechanistically, luteolin causes cell death by downregulating Akt, PLK-1, cyclin-B1, cyclin-A, CDC-2, CDK-2, Bcl-2, and Bcl-xL, while upregulating BAX, caspase-3, and p21. It has also been reported to inhibit STAT3 signaling by the suppression of STAT3 activation and enhanced STAT3 protein degradation in various cancer cells. Therefore, extensive studies on the anticancer properties of luteolin reveal its promising role in chemoprevention. The present review describes all the possible cellular interactions of luteolin in cancer, along with its synergistic mode of action and nanodelivery insight.

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