Magnolol induces apoptosis via activation of both mitochondrial and death receptor pathways in A375-S2 cells

You, Qingjun; Li, Mingqiu; Jiao, Guoqing

doi:10.1007/s12272-009-2218-6

Cited by 18 publications

(18 citation statements)

References 16 publications

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“…1C). These results suggest that Magnolol can act as growth inhibitor of gastric adenocarcinoma SGC-7901 cells in a similar fashion as described in previous studies dealing with various other types of cancer cells including melanoma cells (21), colon cancer cells (24,25), prostrate cancer cells (26,27), human glioblastoma cancer cells (28,29), liver cancer cells (32), lung cancer cells (30,31), leukemic cells (14), thyroid carcinoma cells (33), and human urinary bladder cancer 5637 cells (35). …”

Section: Resultssupporting

confidence: 85%

“…Apoptosis is one of the modes of cell death and induction of apoptosis is the key characteristic of anticancer drugs as it plays an imperative role in the elimination of damaged cells and the maintenance of homeostasis and many of the natural chemopreventive agents, including Magnolol, exert their effect via induction of apoptosis in cancer cells (21,49,50). To elucidate the effect of Magnolol on induction of apoptosis in SGC-7901 cells, these cells were treated with Magnolol and incubated with PI, analysed by flow cytometry and resulted in the increase of subG1 phase which represents the apoptotic cell population.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, Magnolol induced antiproliferative effects in wide variety of tumor cells including melanoma cells (18–21), colon cancer cells (22–25), prostate cancer cells (26,27), human glioblastoma cancer cells (28,29), liver cancer cells (24,25), lung cancer cells (30,31), leukemic cells (14), cervical cancer (32), ovarian cancer cells (32), thyroid carcinoma cells (33), human fibrosarcoma HT-1080 (34), and human urinary bladder cancer 5637 cells (35,36). Several researchers reported that Magnolol-induced cell death involve apoptosis while Li et al (30), reported that Magnolol-induced death occurs via autophagy but not apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Magnolol, a natural compound, induces apoptosis of SGC-7901 human gastric adenocarcinoma cells via the mitochondrial and PI3K/Akt signaling pathways

Rasul

B²,

Khan³

et al. 2011

International Journal of Oncology

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Abstract. Gastric cancer is the fourth most commonly diagnosed cancer with the second highest mortality rate worldwide. Surgery, chemotherapy and radiation therapy are generally used for the treatment of stomach cancer but only limited clinical response is shown by these therapies and still no effectual therapy for advanced gastric adenocarcinoma patients is available. Therefore, there is a need to identify other therapeutic agents against this life-threatening disease. Plants are considered as one of the most important sources for the development of anticancer drugs. Magnolol, a natural compound possesses anticancer properties. However, effects of Magnolol on human gastric cancer remain unexplored. The effects of Magnolol on the viability of SGC-7901 cells were determined by the MTT assay. Apoptosis, mitochondrial membrane potential and cell cycle were evaluated by flow cytometry. Protein expression of Bcl-2, Bax, caspase-3 and PI3K/Akt was analysed by Western blotting. Magnolol induced morphological changes in SGC-7901 cells and its cytotoxic effects were linked with DNA damage, apoptosis and S-phase arrest in a dose-dependent manner. Magnolol triggered the mitochondrial-mediated apoptosis pathway as shown by an increased ratio of Bax/Bcl-2, dissipation of mitochondrial membrane potential (ΔΨm), and sequential activation of caspase-3 and inhibition of PI3K/Akt. Additionally, Magnolol induced autophagy in SGC-7901 cells at high concentration but was not involved in cell death. Magnolol-induced apoptosis of SGC-7901 cells involves mitochondria and PI3K/ Akt-dependent pathways. These findings provide evidence that Magnolol is a promising natural compound for the treatment of gastric cancer and may represent a candidate for in vivo studies of monotherapies or combination antitumor therapies. IntroductionGastric cancer is the second most common cause of cancerrelated death worldwide and approximately 800,000 people die each year of this malignancy. So far it is the fourth most frequently diagnosed cancer as each year more than one million patients are annually diagnosed with gastric cancer (1,2). The incidence of stomach cancer varies geographically, with a much higher prevalence in Eastern countries than in the Western ones (3). In 2005, the incidence of gastric cancer (0.3 million deaths and 0.4 million new cases) ranked third among the most common cancers in China (4). Although surgery remains the gold standard for the treatment of stomach cancer but the limitations is that it is diagnosed at an advanced stage. The 5-year survival rate of patients with advanced gastric cancer for surgical treatment is less than 40%. The effectiveness of chemotherapy and/or radiation therapy, in addition to surgery, has been actively studied over the last few decades. Unfortunately, only a little clinical response is generally shown by chemotherapy or radiation therapy and survival rate is also very poor (5). There is no effective therapy for patients with advanced gastric adenocarcinoma. Therefore, to identify new therapeutic ag...

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Section: Resultssupporting

confidence: 85%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Magnolol, a natural compound, induces apoptosis of SGC-7901 human gastric adenocarcinoma cells via the mitochondrial and PI3K/Akt signaling pathways

Rasul

B²,

Khan³

et al. 2011

International Journal of Oncology

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“…Magnolol induces apoptosis via activation of both mitochondrial and death receptor pathways in A375-S2 malignant melanoma cells [54]. Recent studies by Tanaka et al [55], have shown the preventive effects of magnolol on UV-induced photoaging by inhibiting the expression of NF-kB.…”

Section: Discussionmentioning

confidence: 99%

Effects of magnolol on UVB-induced skin cancer development in mice and its possible mechanism of action

Chilampalli

Guillermo

Zhang³

et al. 2011

BMC Cancer

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BackgroundMagnolol, a plant lignan isolated from the bark and seed cones of Magnolia officinalis, has been shown to have chemopreventive effects on chemically-induced skin cancer development. The objectives of this investigation are to study the anticarcinogenic effects of magnolol on UVB-induced skin tumor development in SKH-1 mice, a model relevant to humans, and determine the possible role of apoptosis and cell cycle arrest involved in the skin tumor development.MethodsUVB-induced skin carcinogenesis model in SKH-1 mice was used for determining the preventive effects of magnolol on skin cancer development. Western blottings and flow cytometric analysis were used to study the effects of magnolol on apoptosis and cell cycle.ResultsMagnolol pretreated groups (30, 60 μ g) before UVB treatments (30 mJ/cm2, 5 days/week) resulted in 27-55% reduction in tumor multiplicity as compared to control group in SKH-1 mice. Magnolol pretreatment increased the cleavage of caspase-8 and poly-(-ADP-ribose) polymerase (PARP), increased the expression of p21, a cell cycle inhibitor, and decreased the expression of proteins involved in the G2/M phase of cell cycle in skin samples from SKH-1 mice.Treatment of A431 cells with magnolol decreased cell viability and cell proliferation in a concentration dependent manner. Magnolol induced G2/M phase cell cycle arrest in A431 cells at 12 h with a decreased expression of cell cycle proteins such as cyclin B1, cyclin A, CDK4, Cdc2 and simultaneous increase in the expression of Cip/p21, a cyclin-dependent kinase inhibitor. Magnolol induced apoptosis in vivo and in vitro with an increased cleavage of caspase-8 and PARP. Phospho-signal transducers and activators of transcription 3 (Tyr705), B-Raf, p-MEK, and p-AKT were down-regulated, whereas phosphorylation of ERK was induced by magnolol in A431 cells.ConclusionsMagnolol pretreatments prevent UVB-induced skin cancer development by enhancing apoptosis, causing cell cycle arrest at G2/M phase, and affecting various signaling pathways. Magnolol could be a potentially safe and potent anticarcinogenic agent against skin cancer.

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“…Furthermore, MAG also suppressed ERK1/2 kinase, MAPK, and the PI3K/AKT pathway in DMBA/TPA-induced skin cancer in female mice [155]. MAG inhibited cell proliferation in the human malignant melanoma A375-S2 cell line by increasing caspases-3, -8,-9 activities, augmenting the expression of anti-apoptotic mitochondrial protein Bcl-2 while decreasing the expression of pro-apoptotic protein Bax [147]. In vivo studies on different animal models of skin cancer demonstrated that MAG reduced tumor growth, induced apoptosis and arrested cell cycle at the G2/M phase (Table 1) [56,156,157].…”

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

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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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Magnolol induces apoptosis via activation of both mitochondrial and death receptor pathways in A375-S2 cells

Cited by 18 publications

References 16 publications

Magnolol, a natural compound, induces apoptosis of SGC-7901 human gastric adenocarcinoma cells via the mitochondrial and PI3K/Akt signaling pathways

Magnolol, a natural compound, induces apoptosis of SGC-7901 human gastric adenocarcinoma cells via the mitochondrial and PI3K/Akt signaling pathways

Effects of magnolol on UVB-induced skin cancer development in mice and its possible mechanism of action

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

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