Apigenin decreases cell viability and telomerase activity in human leukemia cell lines

Jayasooriya, Rajapaksha Gedara Prasad Tharanga; Kang, Sang-Hyuck; Kang, Chang‐Hee; Choi, Yung Hyun; Moon, Dong‐Oh; Hyun, Jin‐Won; Chang, Weon-Young; Kim, Gi‐Young

doi:10.1016/j.fct.2012.05.024

Cited by 53 publications

(38 citation statements)

References 36 publications

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“…At 10 μM, apigenin significantly and near-maximally reduced IL-6 secretion by these normal cells. Because apigenin was shown to induce apoptosis and inhibit cell proliferation in cancer cell lines (Reiners et al 1999, Gupta et al 2001, Way et al 2004, Brusselmans et al 2005, Shukla and Gupta 2007, Jayasooriya et al 2012, we tested it for these activities in normal human fibroblasts. At 10 μM, apigenin did not induce apoptosis in non-senescent or senescent normal cells and, while robustly reducing IL-6 secretion, only decreased proliferation of non-senescent cells by ∼25% while the flavonoid was present.…”

Section: Discussionmentioning

confidence: 99%

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Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells

et al. 2017

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Apigenin (4′,5,7,-trihydroxyflavone) is a flavonoid found in certain herbs, fruits, and vegetables. Apigenin can attenuate inflammation, which is associated with many chronic diseases of aging. Senescent cellsstressed cells that accumulate with age in mammalsdisplay a pro-inflammatory senescence-associated secretory phenotype (SASP) that can drive or exacerbate several age-related pathologies, including cancer. Flavonoids, including apigenin, were recently shown to reduce the SASP of a human fibroblast strain induced to senesce by bleomycin. Here, we confirm that apigenin suppresses the SASP in three human fibroblast strains induced to senesce by ionizing radiation, constitutive MAPK (mitogen-activated protein kinase) signaling, oncogenic RAS, or replicative exhaustion. Apigenin suppressed the SASP in part by suppressing IL-1α signaling through IRAK1 and IRAK4, p38-MAPK, and NF-κB. Apigenin was particularly potent at suppressing the expression and secretion of CXCL10 (IP10), a newly identified SASP factor. Further, apigenin-mediated suppression of the SASP substantially reduced the aggressive phenotype of human breast cancer cells, as determined by cell proliferation, extracellular matrix invasion, and epithelialmesenchymal transition. Our results support the idea that apigenin is a promising natural product for reducing the impact of senescent cells on age-related diseases such as cancer.

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Section: Discussionmentioning

confidence: 99%

“…Apigenin was reported to induce apoptosis of cancer cells (Jayasooriya et al 2012). To determine whether this was the case for normal cells, we treated non-senescent and IRinduced senescent HCA2 cells with DMSO or 10 μM apigenin and assessed apoptosis by activated caspase-3 levels (Fig.…”

Section: Suppression Of Il-6 Expression Upon Apigenin Treatmentmentioning

confidence: 99%

Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells

et al. 2017

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“…Additionally, it was shown that apigenin treatment in a late phase involves the activation of p38 and PKCδ to modulate Hsp27, thus leading to apoptosis [184]. A study by Jayasoorya et al [185] demonstrated that apigenin inhibits cell growth and diminishes telomerase activity in human-derived leukemia cells, ultimately leading to apoptosis. In addition to inducing apoptosis in leukemia cells, apigenin-7 glycoside has been shown to induce granulocyte differentiation that was confirmed by the presence of significant amounts of CD11b positive cells [186].…”

Section: 0 Effect Of Apigenin In Various Human Cancersmentioning

confidence: 99%

Plant Flavone Apigenin: an Emerging Anticancer Agent

et al. 2017

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Research in cancer chemoprevention provides convincing evidence that increased intake of vegetables and fruits may reduce the risk of several human malignancies. Phytochemicals present therein provide beneficial anti-inflammatory and antioxidant properties that serve to improve the cellular microenvironment. Compounds known as flavonoids categorized anthocyanidins, flavonols, flavanones, flavonols, flavones, and isoflavones have shown considerable promise as chemopreventive agents. Apigenin (4′, 5, 7-trihydroxyflavone), a major plant flavone, possessing antioxidant, anti-inflammatory, and anticancer properties affecting several molecular and cellular targets used to treat various human diseases. Epidemiologic and case-control studies have suggested apigenin reduces the risk of certain cancers. Studies demonstrate that apigenin retain potent therapeutic properties alone and/or increases the efficacy of several chemotherapeutic drugs in combination on a variety of human cancers. Apigenin’s anticancer effects could also be due to its differential effects in causing minimal toxicity to normal cells with delayed plasma clearance and slow decomposition in liver increasing the systemic bioavailability in pharmacokinetic studies. Here we discuss the anticancer role of apigenin highlighting its potential activity as a chemopreventive and therapeutic agent. We also highlight the current caveats that preclude apigenin for its use in the human trials.

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“…Recent studies in several biological systems have shown that apigenin possesses anti-proliferative properties, and induces cell cycle arrest and apoptosis in various human and animal-derived cancer cell lines [17]–[20]. In transformed mouse liver cells, apigenin has been reported to reduce the toxicological effects of dioxin by suppressing the dioxin-induced activation of the aryl hydrocarbon receptor [21].…”

Section: Introductionmentioning

confidence: 99%

Plant Flavone Apigenin Binds to Nucleic Acid Bases and Reduces Oxidative DNA Damage in Prostate Epithelial Cells

Kanwal

Bhaskaran

et al. 2014

PLoS ONE

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Oxidative stress has been linked to prostate carcinogenesis as human prostate tissue is vulnerable to oxidative DNA damage. Apigenin, a dietary plant flavone, possesses anti-proliferative and anticancer effects; however, its antioxidant properties have not been fully elucidated. We investigated sub-cellular distribution of apigenin, it’s binding to DNA and protective effects against H2O2-induced DNA damage using transformed human prostate epithelial RWPE-1 cells and prostate cancer LNCaP, PC-3 and DU145 cells. Exposure of cells to apigenin exhibited higher accumulation in RWPE-1 and LNCaP cells, compared to PC-3 and DU145 cells. The kinetics of apigenin uptake in LNCaP cells was estimated with a Km value of 5 µmole/L and Vmax of 190 pmoles/million cells/h. Sub-cellular fractionation demonstrated that nuclear matrix retains the highest concentration of apigenin (45.3%), followed by cytosol (23.9%), nuclear membranes (17.9%) and microsomes (12.9%), respectively. Spectroscopic analysis of apigenin with calf-thymus DNA exhibited intercalation as the dominant binding mode to DNA duplex. Apigenin exposure resulted in significant genoprotective effects in H2O2-stressed RWPE-1 cells by reduction in reactive oxygen species levels. In addition, apigenin exposure suppressed the formation of 8-hydroxy-2′ deoxyguanosine and protected exposed cells from apoptosis. Our studies demonstrate that apigenin is readily taken up by normal prostatic epithelial cells and prostate cancer cells, and is incorporated into their nuclei, where its intercalation with nucleic acid bases may account for its antioxidant and chemopreventive activities.

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Apigenin decreases cell viability and telomerase activity in human leukemia cell lines

Cited by 53 publications

References 36 publications

Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells

Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells

Plant Flavone Apigenin: an Emerging Anticancer Agent

Plant Flavone Apigenin Binds to Nucleic Acid Bases and Reduces Oxidative DNA Damage in Prostate Epithelial Cells

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