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KMID : 1034820220180010009
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Molecular & Cellular Toxicology
2022 Volume.18 No. 1 p.9 ~ p.16
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Glycosidic flavonoids and their potential applications in cancer research: a review
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Abusaliya Abuyaseer
Ha Sang-Eun
Bhosale Pritam Bhagwan
Kim Hun-Hwan
Park Min-Yeong
Vetrivel Preethi
Kim Gon-Sup
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Abstract
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Purpose of review: Every year, the cancer patient registry increases, and the leading cause of death in a global context. Plant-based molecules are gaining attention in cancer research due to the side effects of chemotherapy. A glycosidic derivative of flavonoid (GDF) plays a significant role in cancer proliferation mechanisms. GDF inhibits cell proliferation by elevating the expression of apoptotic proteins, altering the expression of nuclear factor-kappa B (NF- κB), and decreasing mitochondrial membrane potential (Δψm) in cancer cells.
Recent findings: Reported studies on the flavonoids orientin, vitexin, prunetionoside, chrysin, and scutellarein increased attention and are being widely investigated for their potential role in different parts of cancer research. Prunetionoside is a flavonoid with high cytotoxic potential and capable of inducing necroptosis in AGS gastric cancer cells. Similarly, scutellarein is a flavonol, induces an extrinsic apoptotic pathway and downregulates the expression level of cyclin proteins in HepG2 liver cancer cells. Vitexin is reported to be capable of deregulating the expression levels of p-Akt, p-mTOR, and p-PI3K in A549 lung cancer cells. Orientin inhibits IL-8 expression and invasion in MCF-7 breast cancer cells by suppressing MMP-9 in the presence of TPA via STAT3/AP-1/ERK/PKCα-mediated signaling pathways. It also induces mitochondria-mediated intrinsic apoptosis and G0/G1 cell cycle arrest in HT29 colon cancer cells. Chrysin is a flavonoid present in honey that has been shown to play an important role in cervical and colon cancer by suppressing the AKT/mTOR/PI3K pathway and increasing ROS accumulation, LDH leakage, respectively.
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KEYWORD
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Flavonoid, Glycosides, Cancer, Programmed cell death, Cell cycle arrest
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