Cell‐Cycle Arrest at G2/M and Growth Inhibition by Apigenin in Human Colon Carcinoma Cell Lines

Wang, Weiqun; Heideman, Laura J.; Chung, Chilly S.; Pelling, Jill C.; Koehler, Kenneth J.; Birt, Diane F.

doi:10.1002/1098-2744(200006)28:2<102::aid-mc6>3.3.co;2-u

Cited by 60 publications

(75 citation statements)

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“…The mutation of p53 allows the growing tumor to evade cell-cycle arrest at G1 and/or G2/M checkpoints and cause cancer progression (Wang et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Comparison of phototoxic effects of hypericin-mediated photodynamictherapy in HT-29 and Caco-2 colon cancer cells

Süloğlu¹,

Selmanoğlu²,

Yılmaz³

et al. 2016

Turk J Biol

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Hypericin (HYP) is a plant-derived photosensitizer. HYP is preferentially taken up by tumor cells. We designed this study to compare HYP-mediated photodynamic therapy (PDT) in HT-29 and Caco-2 colon cell lines. Cells were treated with 0.04, 0.08, and 0.15 µM HYP concentrations and irradiated. The effect of HYP on metabolic profiles, alterations in lactate dehydrogenase (LDH) leakage, and cell cycle progression was investigated for the first time. Changes in glucose consumption, lactate production, and LDH leakage were analyzed. HYP-induced cell death was quantified by double staining (acridine orange/propidium iodide) and alterations in cell cycle regulation were analyzed with flow cytometry (using propidium iodide). LDH leakage and the number of dead cells were elevated, and glucose consumption and lactate production decreased in a dose-and time-dependent manner. PDT resulted in an induction of apoptosis, mostly at the 0.08 µM HYP concentration. Apoptosis and/or necrosis were increased in the 0.15 µM HYP group. The accumulation of cells in the G2/M phase might account for the growth inhibition in HT-29 and Caco-2 cells with 0.08 µM HYP photoactivation. The observed G2/M arrest suggested that HYP may slow down the growth of colon cancer cells by regulating the cell cycle, leading either to growth inhibition or to initiation of apoptotic pathways.

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“…The mutation of p53 allows the growing tumor to evade cell-cycle arrest at G1 and/or G2/M checkpoints and cause cancer progression (Wang et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Comparison of phototoxic effects of hypericin-mediated photodynamictherapy in HT-29 and Caco-2 colon cancer cells

Süloğlu¹,

Selmanoğlu²,

Yılmaz³

et al. 2016

Turk J Biol

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“…HT-29 cells bear different genetic abnormalities typical of human CRC, such as a mutated Tp53 (Arg 273 His) and a wild-type RAS allele [31].…”

Section: Cells Antibodies and Reagentsmentioning

confidence: 99%

The antiproliferative and proapoptotic effects of cladosporols A and B are related to their different binding mode as PPARγ ligands

Zurlo

Ziccardi

Votino

et al. 2016

Biochemical Pharmacology

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a b s t r a c tCladosporols are secondary metabolites from Cladosporium tenuissimum characterized for their ability to control cell proliferation. We previously showed that cladosporol A inhibits proliferation of human colon cancer cells through a PPARc-mediated modulation of gene expression. In this work, we investigated cladosporol B, an oxidate form of cladosporol A, and demonstrate that it is more efficient in inhibiting HT-29 cell proliferation due to a robust G0/G1-phase arrest and p21 waf1/cip1 overexpression. Cladosporol B acts as a PPARc partial agonist with lower affinity and reduced transactivation potential in transient transfections as compared to the full agonists cladosporol A and rosiglitazone. Site-specific PPARc mutants and surface plasmon resonance (SPR) experiments confirm these conclusions. Cladosporol B in addition displays a sustained proapoptotic activity also validated by p21 waf1/cip1 expression analysis in the presence of the selective PPARc inhibitor GW9662. In the DMSO/H 2 O system, cladosporols A and B are unstable and convert to the ring-opened compounds 2A and 2B. Finally, docking experiments provide the structural basis for full and partial PPARc agonism of 2A and 2B, respectively. In summary, we report here, for the first time, the structural characteristics of the binding of cladosporols, two natural molecules, to PPARc. The binding of compound 2B is endowed with a lower transactivation potential, higher antiproliferative and proapoptotic activity than the two full agonists as compound 2A and rosiglitazone (RGZ).

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“…As neoplastic epithelial cells attain the ability to invade and metastasize, the lesion becomes malignant. Wang et al (89) studied the effects of apigenin on cell growth and the cell cycle in various human colon carcinoma cell lines. Exposure of colon cancer cells to apigenin resulted in cell growth inhibition, followed by reversible G2/M arrest associated with inhibition of p34 (cdc2) kinase, reduced accumulation of p34 (cdc2) and cyclin B1 proteins.…”

Section: Apigenin and Cancermentioning

confidence: 99%

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

Patel

Shukla²,

Gupta³

2007

Int J Oncol

311

362

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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.

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Cell‐Cycle Arrest at G2/M and Growth Inhibition by Apigenin in Human Colon Carcinoma Cell Lines

Cited by 60 publications

References 0 publications

Comparison of phototoxic effects of hypericin-mediated photodynamictherapy in HT-29 and Caco-2 colon cancer cells

Comparison of phototoxic effects of hypericin-mediated photodynamictherapy in HT-29 and Caco-2 colon cancer cells

The antiproliferative and proapoptotic effects of cladosporols A and B are related to their different binding mode as PPARγ ligands

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

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