Tricetin, a Dietary Flavonoid, Inhibits Proliferation of Human Breast Adenocarcinoma MCF-7 Cells by Blocking Cell Cycle Progression and Inducing Apoptosis

Hsu, Ya‐Ling; Uen, Yih-Huei; Chen, Yi; Liang, Hsin-Lin; Kuo, Po‐Lin

doi:10.1021/jf901053x

Cited by 53 publications

(32 citation statements)

References 36 publications

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“…Cell cycle regulatory proteins, including cyclins and CDKs, are considered to serve an important role in cell cycle progression (34). Cyclin A, CDK2 and CDC25A are critical factors associated with the S phase of the cell cycle (35).…”

Section: Discussionmentioning

confidence: 99%

Chloroquine exerts antitumor effects on NB4 acute promyelocytic leukemia cells and functions synergistically with arsenic trioxide

et al. 2017

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Abstract. Chloroquine (CQ) has been confirmed to exhibit antitumor effects on different types of cancer cell, but whether it exerts the same effect on acute promyelocytic leukemia (APL) cells remains to be confirmed. In the present study, the effects of various concentrations of CQ on the growth, apoptosis and cell cycle distribution ofNB4 cells, as well as the potential mechanisms underlying these effects, were examined. The combined effect of CQ and arsenic trioxide (ATO) on the growth of NB4 cells was also determined. The results of the present study demonstrated that CQ treatment inhibited cell proliferation, and induced mitochondrial pathway apoptosis and S phase arrest in a dose-dependent manner by regulating apoptosis-and cell cycle-related proteins. CQ and ATO had a synergistic effect on the growth inhibition of NB4 cells, which may have been induced through the inhibition of autophagy. In conclusion, the results of the present study indicated that CQ exhibits a cytotoxic effect on NB4 cells and has a synergistic effect when combined with ATO, which thereby improves the curative effect of ATO on APL.

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Section: Discussionmentioning

confidence: 99%

Chloroquine exerts antitumor effects on NB4 acute promyelocytic leukemia cells and functions synergistically with arsenic trioxide

et al. 2017

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“…The activity of CDK/cyclin complexes is regulated by PCNA, which binds to the cyclin D1/CDK4 complex, thus promoting progression through the G 1 phase into S phase. CKIs, such as p53, p21, and p27, are tumor suppressor proteins that downregulate cell cycle progression by binding with active cyclin-CDK complexes, thereby inhibiting their activities (Hsu et al 2009). Expression of p53 is upregulated by directly binding to a p53-responsive element in p21 elements.…”

Section: Discussionmentioning

confidence: 99%

Modulatory effect of phytoglycoprotein (38 kDa) on cyclin D1/CDK4 in BNL CL.2 cells induced by N-methyl-N′-nitro-N-nitrosoguanidine

Liu

Lim

2011

Naunyn-Schmiedeberg's Arch Pharmacol

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In the developmental stages of cancer, cell transformation occurs after the promotion stage and is a marker of cancer progression. This cell transformation is related to abnormal proliferation during the cancer initiation stage. The purpose of this study was to evaluate the effect of Styrax japonica Siebold et al. Zuccarin (SJSZ) glycoprotein on cell transformation in murine embryonic liver cells (BNL CL.2) following N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) treatment. To determine abnormal proliferation during the initiation stage, intracellular reactive oxygen species (ROS), phosphorylation of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK), activities of cell cycle-related factors [cyclin D1/cyclin dependent kinase (CDK) 4], cell cycle inhibitors (p53, p21, and p27), nuclear factor (NF)-κB, and proliferating cell nuclear antigen (PCNA) were evaluated using Western blot analysis and real-time PCR. Our study demonstrated that SJSZ glycoprotein (50 μg/ml) reduces foci formation with combined treatment [MNNG and 12-O-tetradecanoyl phorbol-13-acetate] of BNL CL.2 cells. With regard to proliferation-related signals, our finding indicated that SJSZ glycoprotein (50 μg/ml) diminished the production of intracellular ROS, activity of phosphorylated ERK, p38 MAPK, NF-κB (p50 and p65), PCNA, and cyclin D1/CDK4 in MNNG-induced BNL CL.2 cells. Taken together, these results lead us to speculate that SJSZ glycoprotein can inhibit abnormal cell proliferation at the initiation stage of hepatocarcinogenesis.

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“…Tricetin flavonoid, isolated from Eucalyptus honey, was reported to inhibit cell proliferation, induce G2/M arrest, and lead to apoptosis in human breast adenocarcinoma MCF-7 cells (Hsu et al 2009b). After tricetin treatment, both ATM and p53 were activated and the apoptosis signaling proteins were overexpressed in MCF-7 cells.…”

Section: Eucalyptus Honeymentioning

confidence: 99%

Activation and Inhibition of ATM by Phytochemicals: Awakening and Sleeping the Guardian Angel Naturally

Farooqı

Tang

et al. 2015

Arch. Immunol. Ther. Exp.

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Double-stranded breaks (DSBs) are cytotoxic DNA lesions caused by oxygen radicals, ionizing radiation, and radiomimetic chemicals. Increasing understanding of DNA damage signaling has provided an ever-expanding list of modulators reported to orchestrate DNA damage repair and ataxia telangiectasia mutated (ATM) is the master regulator and main transducer of the DSB response. Increasingly, it is being realized that DNA damage response is a synchronized and branched network that functionalizes different molecular cascades to activate special checkpoints, thus temporarily arresting progression of the cell cycle while damage is being assessed and processed. It is noteworthy that both nutrigenetics and nutrigenomics have revolutionized the field of molecular biology and rapidly accumulating experimental evidence has started to shed light on biological activities of a wide range of phytochemicals reported to modulate cell cycle, DNA repair, cell growth, differentiation and apoptosis as evidenced by cell-based studies. In this review, we have attempted to provide an overview of DNA damage signaling, how ATM signaling regulates tumor necrosis factors-related apoptosis inducing ligand (TRAIL)-induced intracellular network. We also illuminate on how resveratrol, epigallocatechin gallate, curcumin, jaceosidin, cucurbitacin, apigenin, genistein, and others trigger activation of ATM in different cancer cells as well as agents for ATM inactivation. Understanding the interplay of TRAIL-induced intracellular signaling and ATM modulation of downstream effectors is very important. This holds particularly for a reconceptualization of the apparently paradoxical roles and therapeutically targetable for enhancing the response to DNA damage-inducing therapy.

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Tricetin, a Dietary Flavonoid, Inhibits Proliferation of Human Breast Adenocarcinoma MCF-7 Cells by Blocking Cell Cycle Progression and Inducing Apoptosis

Cited by 53 publications

References 36 publications

Chloroquine exerts antitumor effects on NB4 acute promyelocytic leukemia cells and functions synergistically with arsenic trioxide

Chloroquine exerts antitumor effects on NB4 acute promyelocytic leukemia cells and functions synergistically with arsenic trioxide

Modulatory effect of phytoglycoprotein (38 kDa) on cyclin D1/CDK4 in BNL CL.2 cells induced by N-methyl-N′-nitro-N-nitrosoguanidine

Activation and Inhibition of ATM by Phytochemicals: Awakening and Sleeping the Guardian Angel Naturally

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