Growth Inhibition and Induction of G1 Phase Cell Cycle Arrest in Human Lung Cancer Cells by a Phenylbutenoid Dimer Isolated from Zingiber cassumunar

Lee, Jong Won; Min, Hye Young; Han, Ah Reum; Chung, Hwa Jin; Park, Eun Jung; Park, Hyen Joo; Hong, Ji Young; Seo, Eun Kyoung; Lee, Sang Kook

doi:10.1248/bpb.30.1561

Cited by 21 publications

(14 citation statements)

References 17 publications

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“…[21][22][23] Cyclin D1, CDK4 and E2F1 are important proteins promoting transition of G 1 to S phase. [24][25][26][27] On the other hand, p27 acts as the inhibitor of transition of G 1 to S phase. [28][29][30] In summary, SAD downregulated the expressions of proteins promoting transition of G 1 /S and upregulated the expressions of proteins inhibiting transition of G 1 /S, which was coincident with PI staining and flow cytometry analysis showing increase of G 1 content.…”

Section: Discussionmentioning

confidence: 99%

Secalonic Acid D induced leukemia cell apoptosis and cell cycle arrest of G1 with involvement of GSK-3β/β-catenin/c-Myc pathway

Zhang¹,

Tao²,

Liang³

et al. 2009

Cell Cycle

101

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Section: Discussionmentioning

confidence: 99%

Secalonic Acid D induced leukemia cell apoptosis and cell cycle arrest of G1 with involvement of GSK-3β/β-catenin/c-Myc pathway

Zhang¹,

Tao²,

Liang³

et al. 2009

Cell Cycle

101

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“…Propolis was shown to inhibit the expression of cyclins B1 and D1, and CDK4, and induce CDKN1A (p21) expression, as indicated in [202]. A novel phenylbutenoid dimer (+/-)-trans-3- (3, 4-dimethoxyphenyl)-4-[(E)-3, 4-dimethoxy-styryl] cyclohex-1-ene (PSC), isolated from Zingiber cassumunar ROXB (Zingiberaceae), inhibited proliferation of various human cancer cells [203]. PSC was shown to induce a cell cycle arrest of human lung cancer A549 cells at the G0/G1 phase, and induce expression of CDKN1A (p21), while reducing expression of cyclins A and D1, CDK-2, and -4, as indicated in [203].…”

Section: Cell Cycle Regulation By Natural Compounds Affecting Cyclinsmentioning

confidence: 99%

“…A novel phenylbutenoid dimer (+/-)-trans-3- (3, 4-dimethoxyphenyl)-4-[(E)-3, 4-dimethoxy-styryl] cyclohex-1-ene (PSC), isolated from Zingiber cassumunar ROXB (Zingiberaceae), inhibited proliferation of various human cancer cells [203]. PSC was shown to induce a cell cycle arrest of human lung cancer A549 cells at the G0/G1 phase, and induce expression of CDKN1A (p21), while reducing expression of cyclins A and D1, CDK-2, and -4, as indicated in [203]. Glycyrrhizin from Japanese herbal supplement ‘Sho-saiko-to’ (also known as minor bupuleurum formula and Xiao Chai Hu Tang in Chinese) was shown to block proliferation of murine malignant melanoma Mel-ret cells in G1 phase by decreasing the expression of CDK-4 and -6 protein levels, as indicated in [204].…”

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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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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“…3, 4 and 5). Some low molecular weight compounds, in particular a penylbutenoid dimer which showed a similar level of 50% inhibitory concentration to the LC compounds (10- 30 μM), induces a G 0 /G 1 phase cell cycle arrest as one of the anti-proliferative mechanisms in A549 cells [16]. In addition, Nguyen et al showed that kaempferol, which is one of flavonoid glycons found in diet, inhibits growth and induces apoptosis via activation of MEK-MAPK and c-Jun [17].…”

Section: Discussionmentioning

confidence: 91%

“…6 and 7). Because mutated Ras protein contributes to the growth of lung cancer cells, G1 phase arrest is thus considered to be one of the important anti-proliferative mechanisms against A549 cell growth as shown in earlier reports [16][17][18][19]. In addition, Yano et al reported that a vitamin E derivative inhibited the mutated K-Ras-ERK pathway and induced G1 arrest and the suppression of proliferation in A549 cells without causing any toxicity in normal cells [19].…”

Section: Discussionmentioning

confidence: 92%

Suppressive effects of liquid crystal compounds on the growth of the A549 human lung cancer cell line

et al. 2010

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The aim of this study was to evaluate the biological activity and pharmacological activity of several amphiphilic liquid-crystalline compounds (LCs), i.e. phenylpyrimidine derivatives possessing D-glucamine and cyanobiphenyl derivatives with a terminal hydroxyl unit, to explore novel anti-cancer functions of the LCs. The anti-cancer properties of the LCs were investigated in A549 human lung cancer cells by assessing cell growth, cell cycle distribution, and cell signaling pathways using a flow cytometer and a Western blot analysis. In addition, the effect of LCs on the growth of WI-38 normal fibroblasts was examined. Consequently, the phenylpyrimidine derivatives and cyanobiphenyl derivatives showed cytostatic effects, causing the suppression of cell growth through G1 phase arrest in A549 cells. Further analyses using phenylpyrimidine derivatives and precursors of a cyanobiphenyl compound demonstrated the structure-activity relationships. One of the phenylpyrimidine derivatives inhibited A549 growth without any toxicity to normal fibroblasts. As a result, a novel pharmacological function was hypothesized to be inherent in the structure of the LCs themselves, and the dependence of the tumor-specific activity on the hydrophobic group of phenylpyrimidine derivatives therefore remains an interesting issue. Our results suggest the possibility that the LCs themselves may act as a novel type of chemotherapeutic agent.

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Growth Inhibition and Induction of G1 Phase Cell Cycle Arrest in Human Lung Cancer Cells by a Phenylbutenoid Dimer Isolated from Zingiber cassumunar

Cited by 21 publications

References 17 publications

Secalonic Acid D induced leukemia cell apoptosis and cell cycle arrest of G1 with involvement of GSK-3β/β-catenin/c-Myc pathway

Secalonic Acid D induced leukemia cell apoptosis and cell cycle arrest of G1 with involvement of GSK-3β/β-catenin/c-Myc pathway

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

Suppressive effects of liquid crystal compounds on the growth of the A549 human lung cancer cell line

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