Effect of derivatives of chrysophanol, a new type of potential antitumor agents of anthraquinone family, on growth and cell cycle of L1210 leukemic cells

Darzynkiewicz, Zbigniew; Carter, S.P.; Kapuściński, Jan; Watanabe, Kyoichi A.

doi:10.1016/0304-3835(89)90128-6

Cited by 8 publications

(2 citation statements)

References 5 publications

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“…Alternatively, alkylation of DNA or other cell constituents has also been thought to be the primary lesion(s) leading to perturbation of the cell cycle. 93 Later, emodin was discovered as a strong inhibitor of a protein tyrosine kinase (p56lck), which was the first report relating emodin to a specific cellular target. 94 Therefore, further studies were initiated to evaluate whether emodin caused inhibition of other tyrosine kinase receptors as well.…”

Section: A N T I T U M O R E M O D I N -U P G R a D A T I O N F R Omentioning

confidence: 99%

Molecular mechanism of emodin action: Transition from laxative ingredient to an antitumor agent

Srinivas

Babykutty

Sathiadevan

et al. 2006

Medicinal Research Reviews

262

139

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Anthraquinones represent a large family of compounds having diverse biological properties. Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a naturally occurring anthraquinone present in the roots and barks of numerous plants, molds, and lichens, and an active ingredient of various Chinese herbs. Earlier studies have documented mutagenic/genotoxic effects of emodin, mainly in bacterial system. Emodin, first assigned to be a specific inhibitor of the protein tyrosine kinase p65lck, has now a number of cellular targets interacting with it. Its inhibitory effect on mammalian cell cycle modulation in specific oncogene overexpressed cells formed the basis of using this compound as an anticancer agent. Identification of apoptosis as a mechanism of elimination of cells treated with cytotoxic agents initiated new studies deciphering the mechanism of apoptosis induced by emodin. At present, its role in combination chemotherapy with standard drugs to reduce toxicity and to enhance efficacy is pursued vigorously. Its additional inhibitory effects on angiogenic and metastasis regulatory processes make emodin a sensible candidate as a specific blocker of tumor-associated events. Additionally, because of its quinone structure, emodin may interfere with electron transport process and in altering cellular redox status, which may account for its cytotoxic properties in different systems. However, there is no documentation available which reviews the biological activities of emodin, in particular, its growth inhibitory effects. This review is an attempt to analyze the biological properties of emodin, a molecule offering a broad therapeutic window, which in future may become a member of anticancer armamentarium.

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Section: A N T I T U M O R E M O D I N -U P G R a D A T I O N F R Omentioning

confidence: 99%

Molecular mechanism of emodin action: Transition from laxative ingredient to an antitumor agent

Srinivas

Babykutty

Sathiadevan

et al. 2006

Medicinal Research Reviews

262

139

View full text Add to dashboard Cite

show abstract

“…Naturally occurring compounds are considered as the most interesting agents to test for cancer prevention and therapy, due to their anticipated multimodal actions and limited toxicity, affecting the signaling pathways within the cells, including regulation of cell proliferation, activation of apoptosis and modulation of cell cycle arrest ( 6 , 7 ). Chrysophanol (1,8-dihydroxy-3-methylanthraquinone), extracted from plants of Rheum genus, is one of the anthraquinone compounds, which has been suggested to induce cell death in different types of cancer cells ( 8 , 9 ). The effects of chrysophanol on human prostate cancer cell death have not been studied.…”

Section: Introductionmentioning

confidence: 99%

Gold-chrysophanol nanoparticles suppress human prostate cancer progression through inactivating AKT expression and inducing apoptosis and ROS generation in vitro and in vivo

Mao

et al. 2017

International Journal of Oncology

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Controlled releasing of regulations remains the most convenient method to deliver various drugs. In the present study, we precipitated gold nanoparticles with chrysophanol. The gold-chrysophanol into poly (DL-lactide-co-glycolide) nanoparticles was loaded and the biological activity of chrysophanol nanoparticles on human LNCap prostate cancer cells, was tested to acquire the sustained releasing property. The circular dichroism spectroscopy indicated that chrysophanol nanoparticles effectively resulted in conformational alterations in DNA and regulated different proteins associated with cell cycle arrest. The reactive oxygen species (ROS), apoptosis, cell cycle, DNA damage, Cyto-c and caspase-3 activity were analyzed, and the expression levels of different anti- and pro-apoptotic were studied using immunoblotting analysis. The cytotoxicity assay suggested that chrysophanol nanoparticles preferentially killed prostate cancer cells in comparison to the normal cells. Chrysophanol nanoparticles reduced histone deacetylases (HDACs) to suppress cell proliferation and induce apoptosis by arresting the cell cycle in sub-G phase. In addition, the cell cycle-related proteins, including p27, CHK1, cyclin D1, CDK1, p-AMP-activated protein kinase (AMPK) and p-protein kinase B (AKT), were regulated by chrysophanol nanoparticles to prevent human prostate cancer cell progression. Chrysophanol nanoparticles induced apoptosis in LNCap cells by promoting p53/ROS crosstalk to prevent proliferation. Pharmacokinetic study in mice indicated that chrysophanol nanoparticle injection showed high bioavailability compared to the free chrysophanol. Also, in vivo study revealed that chrysophanol nanoparticles obviously reduced tumor volume and weight. In conclusion, the data above suggested that chrysophanol nanoparticles might be effective to prevent human prostate cancer progression.

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RETRACTED ARTICLE: Chrysophanol suppresses growth and metastasis of T cell acute lymphoblastic leukemia via miR-9/PD-L1 axis

Yin

Liang

et al. 2019

Naunyn-Schmiedeberg's Arch Pharmacol

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Effect of derivatives of chrysophanol, a new type of potential antitumor agents of anthraquinone family, on growth and cell cycle of L1210 leukemic cells

Cited by 8 publications

References 5 publications

Molecular mechanism of emodin action: Transition from laxative ingredient to an antitumor agent

Molecular mechanism of emodin action: Transition from laxative ingredient to an antitumor agent

Gold-chrysophanol nanoparticles suppress human prostate cancer progression through inactivating AKT expression and inducing apoptosis and ROS generation in vitro and in vivo

RETRACTED ARTICLE: Chrysophanol suppresses growth and metastasis of T cell acute lymphoblastic leukemia via miR-9/PD-L1 axis

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