Anticancer potential of magnolol for lung cancer treatment

Seo, Jae-Uk; Kim, Minho; Kim, Hyung-Min; Jeong, Hyun‐Ja

doi:10.1007/s12272-011-0413-8

Cited by 28 publications

(19 citation statements)

References 36 publications

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“…Furthermore, it also increases the expression of the genes involved in malignant conversion and tumor promotion [8,63,106,107,108,109,110,111,112,113,114,115]. It is now well known that the primary targets of MAG are NF-κB and NF-κB regulated proteins and that MAG induces cell death and reduces cell proliferation by inhibition of NF-κB activity [116,117,118]. MAG prevents invasion and migration of cancer cells by reversal of epithelial-mesenchymal transition (EMT) via inhibition of NF-κB activation.…”

Section: Molecular Targets Of Magnololmentioning

confidence: 99%

“…Seo J.U. et al, in 2011, revealed that MAG can alter the cell cycle in A549 cells and can also mediate caspase-dependent apoptosis via downregulation of NF-κB/Rel A in the nucleus [118]. Another study on small lung cancer H460 cells demonstrated that MAG initiates cell death via autophagy instead of apoptosis [120].…”

Section: Effect Of Magnolol In Different Cancersmentioning

confidence: 99%

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Magnolol: A Neolignan from the Magnolia Family for the Prevention and Treatment of Cancer

Ranaware¹,

Banik

Deshpande³

et al. 2018

IJMS

138

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The past few decades have witnessed widespread research to challenge carcinogenesis; however, it remains one of the most important health concerns with the worst prognosis and diagnosis. Increasing lines of evidence clearly show that the rate of cancer incidence will increase in future and will create global havoc, designating it as an epidemic. Conventional chemotherapeutics and treatment with synthetic disciplines are often associated with adverse side effects and development of chemoresistance. Thus, discovering novel economic and patient friendly drugs that are safe and efficacious is warranted. Several natural compounds have proved their potential against this dreadful disease so far. Magnolol is a hydroxylated biphenyl isolated from the root and stem bark of Magnolia tree. Magnolol can efficiently prevent or inhibit the growth of various cancers originating from different organs such as brain, breast, cervical, colon, liver, lung, prostate, skin, etc. Considering these perspectives, the current review primarily focuses on the fascinating role of magnolol against various types of cancers, and the source and chemistry of magnolol and the molecular mechanism underlying the targets of magnolol are discussed. This review proposes magnolol as a suitable candidate that can be appropriately designed and established into a potent anti-cancer drug.

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Section: Molecular Targets Of Magnololmentioning

confidence: 99%

Section: Effect Of Magnolol In Different Cancersmentioning

confidence: 99%

Magnolol: A Neolignan from the Magnolia Family for the Prevention and Treatment of Cancer

Ranaware¹,

Banik

Deshpande³

et al. 2018

IJMS

138

View full text Add to dashboard Cite

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“…17, 18 Magnolol induces apoptosis in the cells of many human cancers, including gallbladder cancer, non-small cell lung cancer, prostate cancer, human breast cancer, bladder cancer, colon cancer, and skin cancer. 9, 10, 11, 12, 14, 18, 19, 20, 21, 22, 23, 24 Therefore, magnolol has been suggested as a potential apoptosis-targeting drug. 25 Together, the results from the existing in vivo and in vitro studies have indicated that magnolol is a promising candidate for the development of new strategies for preventing and/or treating skin cancers in humans.…”

mentioning

confidence: 99%

2-O-Methylmagnolol upregulates the long non-coding RNA, GAS5, and enhances apoptosis in skin cancer cells

et al. 2017

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Magnolol, a hydroxylated biphenol compound isolated from the bark of Magnolia officinalis, has been shown to exhibit anti-proliferative effect in various cancer cells, including skin cancer cells. Methoxylation of magnolol appears to improve its anti-inflammatory activity, yet the effect of this modification on the agent's antitumor activity remains unknown. In this work, we report that 2-O-methylmagnolol (MM1) displays improved antitumor activity against skin cancer cells compared to magnolol both in vitro and in vivo. The increased antitumor activity of MM1 appears to correlate with its increased ability to induce apoptosis. DNA microarray and network pathway analyses suggest that MM1 affects certain key factors involved in regulating apoptosis and programmed cell death. Interestingly, the level of the long non-coding (lnc) RNA of growth arrest-specific 5 (GAS5) was increased in MM1-treated cells, and inhibition of lncRNA GAS5 inhibited MM1-induced apoptosis. Conversely, overexpression of lncRNA GAS5 inhibited cell proliferation and promoted cell apoptosis in skin cancer cells. The expression of lncRNA GAS5 in the skin cancer tissues was found to be lower than that in the adjacent normal tissues in a majority of patients. Taken together, our findings suggest that MM1 has improved antitumor activity in skin cancer cells, and that this is due, at least in part, to the upregulation of lncRNA GAS5 and the enhancement of apoptosis.

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“…[7] Cells were passaged after reaching confluence every 7-10 days, and passage numbers from 4 to 6 were used for experiments. [8]…”

Section: Methodsmentioning

confidence: 99%

Concentration-dependent differential effects of udenafil on viability, proliferation, and apoptosis in vascular endothelial and smooth muscle cells

Fang

Song²,

So³

et al. 2014

Indian J Pharmacol

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Objectives:Local strategies directed against vascular smooth muscle cell (VSMC) proliferation, such as drug-eluting stents (DES), reduce the occurrence of restenosis. However, these approaches may also inhibit vascular endothelial cell (VEC) proliferation and impair reendothelialization, and hence, increase susceptibility to late thrombosis. In this study we examined the differential effects of various concentrations of the type 5 phosphodiesterase (PDE-5) inhibitor, udenafil, on viability, proliferation, and apoptosis of VEC and VSMC, in order to identify the optimal concentration of udenafil that minimizes inhibition of VEC survival and growth, and maximizes inhibition of VSMC survival and growth.Materials and Methods:VEC from human umbilical veins and VSMC from human aorta were exposed to various concentrations of udenafil (1, 10, and 100 μmol/l and 1 mmol/l) for 24 h, and its effects on cell viability, proliferation, and apoptosis were studied using 5-bromo-2’- deoxyuridine (BrdU), methylthiazoletetrazolium (MTT) assay, trypan blue dye exclusion, and flow cytometry.Results:Udenafil inhibited the survival and growth of VEC and VSMC in a concentration-dependent manner over a range of concentrations. At 100 μmol/l, udenafil, inhibited VEC proliferation significantly less than VSMC proliferation (P < 0.05), and could significantly induce VEC apoptosis less than VSMC apoptosis (P < 0.05).Conclusions:Udenafil has a differential effect on survival and growth in VEC and VSMC. The maximal differential effect, with minimal inhibition of VEC and maximal inhibition of VSMC, occurs at 100 μmol/l. This characteristic suggests that udenafil is a promising agent for use in DES.

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Anticancer potential of magnolol for lung cancer treatment

Cited by 28 publications

References 36 publications

Magnolol: A Neolignan from the Magnolia Family for the Prevention and Treatment of Cancer

Magnolol: A Neolignan from the Magnolia Family for the Prevention and Treatment of Cancer

2-O-Methylmagnolol upregulates the long non-coding RNA, GAS5, and enhances apoptosis in skin cancer cells

Concentration-dependent differential effects of udenafil on viability, proliferation, and apoptosis in vascular endothelial and smooth muscle cells

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