Novel histone deacetylase inhibitors derived from Magnolia officinalis significantly enhance TRAIL-induced apoptosis in non-small cell lung cancer

Liu, Yuting; Tong, Yunli; Xia, Yang; Li, Fangyuan; Zheng, Liang; Liu, Wenqin; Wu, Jinjun; Ou, Rilan; Zhang, Guiyu; Hu, Ming; Liu, Zhongqiu; Lu, Linlin

doi:10.1016/j.phrs.2016.05.028

Cited by 31 publications

(16 citation statements)

References 50 publications

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“…In vitro studies on A549 and H1299 cells showed that MAG causes cell cycle arrest at the G0/G1 phase while simultaneously upregulating pro-apoptotic proteins expression, including TRAIL-R2 (DR5), Bax, caspase-3, cleaved caspase-3, and cleaved PARP. Further, in the same study, the scientists reported that in vivo A549 xenograft model upon treatment with MAG suppressed tumor growth and induced apoptosis by epigenetically activating DR5, which in turn activated death receptor-mediated apoptosis [145]. Seo J.U.…”

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

134

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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: 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

134

View full text Add to dashboard Cite

show abstract

“…Cisplatin, a highly effective and widely used chemotherapeutic agent [21]. Cisplatin can block the synthesis of DNA, thereby blocking the division of cancer cells, is a non-specific choice of broad-spectrum anti-cancer drugs, commonly used in the treatment of NSCLC lung cancer [22]. Several mechanisms account for the cisplatin-resistant of tumor cells have been described.…”

Section: Discussionmentioning

confidence: 99%

The critical role of HDAC1 activates NSCLC growth by nicotine resistance Cisplatin

Peng

2020

Preprint

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Nicotine is active in highly cisplatin-resistant cancer cells; however, there is little evidence for its resistant activity in lung cancer with cisplatin. Many mechanisms of cisplatin resistance have been proposed. The mechanisms of the nicotine treatment of cisplatin-resistant lung cancer for histone deacetylase 1 (HDAC1) activity is unknown. Nicotine was used to analyze cisplatin-resistant non-small cell lung cancer (NSCLC) cancer cell growth. Western blot was used to analyze cell cycle-related proteins. Cancer cell viability (cell survival) was measured with MTT assay. HDAC1 transfected NSCLC cells were used to analyze the direct binding between cytosol and nucleus distribution. Here, using cell viability and migration methods we firstly found nicotine regulated cisplatin-resistant NSCLC cells growth by targeting HDAC1. Expression of cisplatin was negatively correlated with HDAC1. And HDAC1 inhibitor, VPA, in the NSCLC cancer cells were predicted. Further experiments confirmed that HDAC1 directly targeted E2F and cisplatin. Besides, HDAC1 and cisplatin inhibited NSCLC cell growth and reduced expression of E2F and Cyclin E proteins. The use of nicotine compromised cisplatin-induced E2F suppression and cancer cell growth. NSCLC cancer cells co-transfected with nicotine and HDAC1 had a higher cell cycle proliferation. Taken all together, cisplatin interferes with DNA replication kills the cancer cell fastest proliferation; however, nicotine increased detoxification of cisplatin, inhibition of apoptosis and DNA repair, induced cisplatin resistance.

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“…The cytotoxic effects of EVO on NSCLC (A549 and H1299) cells and normal embryonic fibroblast (MRC-5) cells were determined by the MTT assay ( Liu et al, 2016 ). Cells were treated with EVO (0–40 μM) or vehicle for 48 or 72 h. The IC 50 value of EVO was calculated using the GraphPad Prism software (version 5.0, CA, United States) for each cell line.…”

Section: Methodsmentioning

confidence: 99%

Evodiamine, a Novel NOTCH3 Methylation Stimulator, Significantly Suppresses Lung Carcinogenesis in Vitro and in Vivo

Xia

Deng

et al. 2018

Front. Pharmacol.

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Lung cancer is a leading cause of cancer-related deaths worldwide. NOTCH3 signaling is mainly expressed in non-small cell lung carcinoma (NSCLC), and has been proposed as a therapeutic target of NSCLC. While, few agents for preventing or treating NSCLC via targeting NOTCH3 signaling are used in modern clinical practice. Evodiamine (EVO), an alkaloid derived from Euodiae Fructus, possesses low toxicity and has long been shown to exert anti-lung cancer activity. However, the underlying anti-lung cancer mechanisms of EVO are not yet fully understood. In this study, we explored the involvement of NOTCH3 signaling in the anti-lung cancer effects of EVO. Urethane-induced lung cancer mouse model and two NSCLC cell models, A549 and H1299, were used to evaluate the in vivo and in vitro anti-lung cancer action of EVO. A DNA methyltransferase inhibitor was employed to investigate the role of NOTCH3 signaling in the anti-lung cancer effects of EVO. Results showed that EVO potently reduced tumor size and tumor numbers in mice, and inhibited NOTCH3 in the tumors. EVO also dramatically reduced cell viability, induced G2/M cell cycle arrest, inhibited cell migration and reduced stemness in cultured NSCLC cells. Mechanistic studies showed that EVO potently inhibited NOTCH3 signaling by activation of DNMTs-induced NOTCH3 methylation. Importantly, inhibition of NOTCH3 methylation in NSCLC cells diminished EVO’s anti-NSCLC effects. Collectively, EVO, a novel NOTCH3 methylation stimulator, exerted potent anti-lung cancer effects partially by inhibiting NOTCH3 signaling. These findings provide new insight into the EVO’s anti-NSCLC action, and suggest a potential role of EVO in lung cancer prevention and treatment.

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Novel histone deacetylase inhibitors derived from Magnolia officinalis significantly enhance TRAIL-induced apoptosis in non-small cell lung cancer

Cited by 31 publications

References 50 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

The critical role of HDAC1 activates NSCLC growth by nicotine resistance Cisplatin

Evodiamine, a Novel NOTCH3 Methylation Stimulator, Significantly Suppresses Lung Carcinogenesis in Vitro and in Vivo

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