Luteolin, a flavonoid, as an anticancer agent: A review.
By M. Imran, A. Rauf, Tareq Abu-Izneid, M. Nadeem, M. Shariati, I. Khan, A. Imran, I. Orhan, M. Rizwan, M. Atif and 2 more. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2019
827 citations recorded by the source corpus.
Many food-derived phytochemicals and their derivatives represent a cornucopia of new anti-cancer compounds. Luteolin (3,4,5,7-tetrahydroxy flavone) is a flavonoid found in different plants such as vegetables, medicinal herbs, and fruits. It acts as an anticancer agent against various types of human malignancies such as lung, breast, glioblastoma, prostate, colon, and pancreatic cancers. It also blocks cancer development in vitro and in vivo by inhibition of proliferation of tumor cells, protection from carcinogenic stimuli, and activation of cell cycle arrest, and by inducing apoptosis through different signaling pathways. Luteolin can additionally reverse epithelial-mesenchymal transition (EMT) through a mechanism that involves cytoskeleton shrinkage, induction of the epithelial biomarker E-cadherin expression, and by down-regulation of the mesenchymal biomarkers N-cadherin, snail, and vimentin. Furthermore, luteolin increases levels of intracellular reactive oxygen species (ROS) by activation of lethal endoplasmic reticulum stress response and mitochondrial dysfunction in glioblastoma cells, and by activation of ER stress-associated proteins expressions, including phosphorylation of eIF2α, PERK, CHOP, ATF4, and cleaved-caspase 12. Accordingly, the present review article summarizes the progress of recent research on luteolin against several human cancers.
Subfields: Cancer Research, Epidemiology, Oncology
View Paper: https://www.semanticscholar.org/paper/85dea5fe54843243e99b78e7a7ea508bc4189080
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In Cancer Research
Citations in the corpus
- The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges (2019, background): “Luteolin has been reported to reverse EMT by involving the upregulation of E-cadherin expression and downregulation of N-cadherin, SNAIL, and vimentin expression [255].”