The Chemopreventive Bioflavonoid Apigenin Modulates Signal Transduction Pathways in Keratinocyte and Colon Carcinoma Cell Lines

Dross, Rukiyah Van; Xue, Yue; Knudson, Alexandra; Pelling, Jill C.

doi:10.1093/jn/133.11.3800s

Cited by 75 publications

(52 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We also showed that apigenin can induce reversible G 2 -M cell cycle arrest (27), and that G 2 -M arrest was accompanied by inhibition of the p34(cdc2) cyclin-dependent kinase protein level and activity in a p21(waf1)-independent manner (28). Van Dross et al (29) showed apigenin treatment can activate extracellular signal-regulated kinase 1/2, p38 mitogen-activated protein kinase pathways, and downstream transcriptional activators in 308 keratinocytes and human colon carcinoma cell line HCT116.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of UVB-Induced Apoptosis by Apigenin in Human Keratinocytes and Organotypic Keratinocyte Cultures

et al. 2008

Self Cite

View full text Add to dashboard Cite

Topical application of the bioflavonoid 4 ¶,5,7-trihydroxyflavone (apigenin) to mouse skin effectively reduces the incidence and size of skin tumors caused by UVB exposure. The ability to act as a chemopreventive compound indicates that apigenin treatment alters the molecular events initiated by UVB exposure; however, the effects of apigenin treatment on UVB-irradiated keratinocytes are not fully understood. In the present study, we have used three models of human keratinocytes to study the effect of apigenin treatment on UVB-induced apoptosis: HaCaT human keratinocyte cells, primary keratinocyte cultures isolated from human neonatal foreskin, and human organotypic keratinocyte cultures. Each keratinocyte model was exposed to a moderate dose of UVB (300-1,000 J/m 2 ), then treated with apigenin (0-50 Mmol/L), and harvested to assess apoptosis by Western blot analysis for poly(ADP)ribose polymerase cleavage, annexin-V staining by flow cytometry, and/or the presence of sunburn cells. Apigenin treatment enhanced UVB-induced apoptosis >2-fold in each of the models tested. When keratinocytes were exposed to UVB, apigenin treatment stimulated changes in Bax localization and increased the release of cytochrome c from the mitochondria compared with UVB exposure alone. Overexpression of the antiapoptotic protein Bcl-2 and expression of a dominant-negative form of Fas-associated death domain led to a reduction in the ability of apigenin to enhance UVB-induced apoptosis. These results suggest that enhancement of UVB-induced apoptosis by apigenin treatment involves both the intrinsic and extrinsic apoptotic pathways. The ability of apigenin to enhance UVBinduced apoptosis may explain, in part, the photochemopreventive effects of apigenin. [Cancer Res 2008;68(8):3057-65]

show abstract

Section: Discussionmentioning

confidence: 99%

Enhancement of UVB-Induced Apoptosis by Apigenin in Human Keratinocytes and Organotypic Keratinocyte Cultures

et al. 2008

Self Cite

View full text Add to dashboard Cite

show abstract

“…Yarrow ( apigenin prior to a carcinogenic insult has been shown to afford a protective effect in murine skin and colon cancer models (36,37). Apigenin is a strong inhibitor of ornithine decarboxylase, an enzyme that plays a major role in tumor promotion (38).…”

Section: Achillea Millefoliummentioning

confidence: 99%

“…Inhibition of CK2 in HCT-116 and HT-29 cells with the use of two specific CK2 inhibitors, DRB and apigenin, affected a synergistic reduction in cell survival when used in conjunction with TNF·. Van Dross et al (37) demonstrated that the chemopreventive activity of apigenin may be mediated by its ability to modulate the MAPK cascade. Apigenin induced a dose-dependent phosphorylation of both ERK and p38 kinase but had little effect on the phosphorylation of c-jun amino terminal kinase (JNK).…”

Section: Apigenin and Cancermentioning

confidence: 99%

Apigenin and cancer chemoprevention: Progress, potential and promise (Review)

Patel

Shukla²,

Gupta³

2007

Int J Oncol

296

362

View full text Add to dashboard Cite

Abstract. Cancer is one of the major public health burdens in the United States and in other developed countries, causing approximately 7 million deaths every year worldwide. Cancer rates vary dramatically in different regions and populations around the globe, especially between developing and developed nations. Changes in cancer prevalence patterns occur within regions as their populations age or become progressively urbanized. Migration has also contributed to such variations as changes in dietary habits influence cancer rates. These epidemiologic findings strongly suggest that cancer rates are influenced by environmental factors including diet, which is largely preventable. Approaches to prevent cancer include overlapping strategies viz. chemoprevention or dietary cancer prevention. Chemoprevention aims at prevention or reversal of the initiation phase of carcinogenesis or arrest at progression of carcinogenesis through the administration of naturally occurring constituents or pharmacological agents. Cancer prevention through diet may be largely achievable by increased consumption of fruits and vegetables. Considerable attention has been devoted to identifying plant-derived dietary agents which could be developed as promising chemopreventives. One such agent is apigenin. A naturally occurring plant flavone (4', 5, 7,-trihydroxyflavone) abundantly present in common fruits and vegetables including parsley, onions, oranges, tea, chamomile, wheat sprouts and some seasonings. Apigenin has been shown to possess remarkable anti-inflammatory, antioxidant and anti-carcinogenic properties. In the last few years, significant progress has been made in studying the biological effects of apigenin at cellular and molecular levels. This review examines the cancer chemopreventive effects of apigenin in an organ-specificity format, evaluating its limitations and its considerable potential for development as a cancer chemopreventive agent.

show abstract

“…German Chamomile called Matricaria chamomilla which considered the more potent and received more scientific evaluation (Ragaa et al 2011). Some chamomile biological effects were confirmed in experimental models and clinical studies (Vandross et al 2003, Fabian et al 2011). The dried flowers of chamomile contain many terpenoids and flavonoids that contribute to its medicinal properties (Janmejai et al 2010).…”

Section: Introductionmentioning

confidence: 90%

“…There are different preparations of chamomile that have developed; the most popular one is in the form of herbal tea. Biological effects of chamomile have been confirmed in different experimental models and clinical studies (Vandross et al 2003) Ceftriaxone is a bactericidal cephalosporin which is a thirdgeneration, resistant to various types of bacterial β-lactamases; it has effect against Gram-negative and Gram-positive bacteria including Enterobavteriaceae, Haemophilus influenza, Streptococcospnemoniae (Matsuzaki et al 2005). Ceftriaxone inhibit enzymes that are called transpeptidase enzymes which are responsible for the final step in bacterial cell wall synthesis which has significant stability against beta-hydrolysis (Neu.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of Matricaria Chamomilla extract on hepatic-renal toxicity of ceftriaxone in rats

Farouk¹,

Abo-Kora²,

Ali³

2017

IJPT

View full text Add to dashboard Cite

The effect of Matricaria chamomilla (M.chamomilla) against hepatic-renal toxicity of Ceftriaxone was investigated in this study. Twenty eight rats were divided into four groups. The 1 st group was injected with saline as control, the 2 nd and 3 rd groups were injected with M.chamomilla extraction ( 50mg/kg.b.wt) andwith ceftriaxone ( 180 mg/kg.b.wt.) for two and one week respectively while the 4 th group was injected with M.chamomilla extraction plus ceftriaxone. at dose 50mg/kg and 180 mg/kg.b.wt respectively ,daily for the one week and with M.chamomilla extraction only at dose 50mg/kg.b.wt for another week. At the end of the 1 st week, the 3 rd group had significantly higher ALP,ALT,AST, urea and creatinine levels with significantly lower albumin and A/G ratio levels than that of the 1 st and2 nd groups , while the 4 th group did not differ from 1 st and 2 nd groups in terms of these parameters. Histopathological studies revealed that, the 3 rd group had some pathological changes in the liver and kidney. From this study we can conclude that, M. chamomilla extraction can reduce hepatic-renal toxicity of ceftriaxone in rats.

show abstract

The Chemopreventive Bioflavonoid Apigenin Modulates Signal Transduction Pathways in Keratinocyte and Colon Carcinoma Cell Lines

Cited by 75 publications

References 16 publications

Enhancement of UVB-Induced Apoptosis by Apigenin in Human Keratinocytes and Organotypic Keratinocyte Cultures

Enhancement of UVB-Induced Apoptosis by Apigenin in Human Keratinocytes and Organotypic Keratinocyte Cultures

Apigenin and cancer chemoprevention: Progress, potential and promise (Review)

Protective effect of Matricaria Chamomilla extract on hepatic-renal toxicity of ceftriaxone in rats

Contact Info

Product

Resources

About