Induction of G2/M phase arrest by squamocin in chronic myeloid leukemia (K562) cells

Lu, Mei; Yang, Sheng Huei; Hwang, Shiuh Lin; Lu, Yu Jhang; Lin, Yuehui; Wang, Sen Ren; Wu, Yang Chang; Lin, Shinne Ren

doi:10.1016/j.lfs.2005.09.048

Cited by 30 publications

(18 citation statements)

References 23 publications

(28 reference statements)

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“…The extract was shown to downregulate the protein levels of cyclin A and B1, upregulate the CDKN1A (p21WAF1) and CDKN1B (p27KIP1) protein levels, increase in CDC25C phosphorylation/inactivation, as indicated elsewhere [221]. Squamocin, one of the Annonaceous acetogenins, was shown to inhibit the growth of human immortalized myelogenous leukemia K562 cells by inducing cell cycle arrest in G2/M phase [222]. Squamocin exposure increased the expression of CDKN1A (p21) and CDKN1B (p27), but decreased the protein levels of CDK1 and CDC25C, as indicated in [222].…”

Section: Cell Cycle Regulation By Natural Compounds Affecting Cyclinsmentioning

confidence: 99%

“…Squamocin, one of the Annonaceous acetogenins, was shown to inhibit the growth of human immortalized myelogenous leukemia K562 cells by inducing cell cycle arrest in G2/M phase [222]. Squamocin exposure increased the expression of CDKN1A (p21) and CDKN1B (p27), but decreased the protein levels of CDK1 and CDC25C, as indicated in [222]. …”

Section: Cell Cycle Regulation By Natural Compounds Affecting Cyclinsmentioning

confidence: 99%

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Natural Compounds as Modulators of Cell Cycle Arrest: Application for Anticancer Chemotherapies

et al. 2017

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Natural compounds from various plants, microorganisms and marine species play an important role in the discovery novel components that can be successfully used in numerous biomedical applications, including anticancer therapeutics. Since uncontrolled and rapid cell division is a hallmark of cancer, unraveling the molecular mechanisms underlying mitosis is key to understanding how various natural compounds might function as inhibitors of cell cycle progression. A number of natural compounds that inhibit the cell cycle arrest have proven effective for killing cancer cells in vitro, in vivo and in clinical settings. Significant advances that have been recently made in the understanding of molecular mechanisms underlying the cell cycle regulation using the chemotherapeutic agents is of great importance for improving the efficacy of targeted therapeutics and overcoming resistance to anticancer drugs, especially of natural origin, which inhibit the activities of cyclins and cyclin-dependent kinases, as well as other proteins and enzymes involved in proper regulation of cell cycle leading to controlled cell proliferation.

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Section: Cell Cycle Regulation By Natural Compounds Affecting Cyclinsmentioning

confidence: 99%

Section: Cell Cycle Regulation By Natural Compounds Affecting Cyclinsmentioning

confidence: 99%

Natural Compounds as Modulators of Cell Cycle Arrest: Application for Anticancer Chemotherapies

et al. 2017

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“…This was determined by [3-(4,5-dime-thylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT, Sigma) assay and also assessed by trypan blue dye exclusion method (Lu et al, 2006).…”

Section: Cell Viability (Bernhard Et Al 2003)mentioning

confidence: 99%

Apoptosis of Human Burkitt’s lymphoma cells induced by 2-N,N-Diethylaminocarbonyloxymethyl-1-diphenylmethyl-4-(3,4,5-trimethoxybenzoyl) piperazine hydrochloride (PMS-1077)

Wang

Chen

et al. 2009

Arch. Pharm. Res.

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Piperazine is one of the heterocycles which are associated with diverse pharmacological activities. 2-N,N-Diethylaminocarbonyloxymethyl-1-diphenylmethyl-4-(3,4,5-trimethoxybenzoyl) piperazine hydrochloride (PMS-1077) is a trisubstituted piperazine which contains a trimethoxybenzene ring and a benzhydrylpiperazine fragment, both of which can induce cell proliferation regression by different mechanisms. We have therefore examined the effects of PMS-1077 on Human Burkitt's lymphoma cells (Raji). The viability of Raji cells was determined by MTT assay and also assessed by trypan blue dye exclusion method. The results demonstrate that PMS-1077 can suppress the proliferation of Raji cells in a dose- and timedependent manner, while inhibit colony formation ability of Raji cells merely in a dose-dependent manner in vitro. Meanwhile, morphological changes were observed using fluorescence microscope. Flow cytometric analysis through PI stains showed that PMS-1077 blocked the growth of Raji cells in the G(0)/G(1) period, and induced apoptosis of Raji cells after 48 h of incubation. Cell apoptosis induced by PMS-1077 was further confirmed by staining with Annexin-V FITC and PI. Preliminary study by molecular docking suggests that PMS-1077 may inhibit tubulin polymerization. More experiments are in progress in our laboratory to reveal the mode of action of PMS-1077 in the induction of apoptosis of Raji cells.

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“…In addition, squamocin (3) was also observed to arrest the same cancer cells at the G1 phase and cause a selective cytotoxicity in S-phase-enriched T24 cells via the same pathway of cleaving the functional protein of PARP and inducing cell apoptosis [74]. Squamocin (3) was also found to inhibit the proliferation of K562 cells via G2/M arrest in association with the induction of p21, p27 and the reduction of Cdk1 and Cdc25C kinase activities [75]. These works connected the AGEs with cell apoptosis, which exploited the multiple functions of AGEs as new anticancer candidates.…”

Section: Biological Activities and The Mechanisms Of Action Of The Agesmentioning

confidence: 96%

Historic Perspectives on Annonaceous Acetogenins from the Chemical Bench to Preclinical Trials

Liaw¹,

Wu²,

Chang³

et al. 2010

Planta Med

Self Cite

111

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Studies on the Annonaceous acetogenins began after the first cytotoxic acetogenin, uvaricin, was isolated in 1982. This attractive finding made many medicinal and natural product chemists direct their efforts on the isolation and identification of these classes of compounds. As more Annonaceous acetogenins were isolated, more information about them was uncovered. From their structural identification to the total synthesis of natural product analogues and from cell-based screening and molecular-based targeting to animal testing, the mechanisms of action of the Annonaceous acetogenins became clearer. The purpose of this review is to give an account of recent studies on this class of compounds and their analogues, which will aid us not only in clarifying how the Annonaceous acetogenins act but also in establishing principles for the further development of this class of compounds

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Induction of G2/M phase arrest by squamocin in chronic myeloid leukemia (K562) cells

Cited by 30 publications

References 23 publications

Natural Compounds as Modulators of Cell Cycle Arrest: Application for Anticancer Chemotherapies

Natural Compounds as Modulators of Cell Cycle Arrest: Application for Anticancer Chemotherapies

Apoptosis of Human Burkitt’s lymphoma cells induced by 2-N,N-Diethylaminocarbonyloxymethyl-1-diphenylmethyl-4-(3,4,5-trimethoxybenzoyl) piperazine hydrochloride (PMS-1077)

Historic Perspectives on Annonaceous Acetogenins from the Chemical Bench to Preclinical Trials

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