Anticancer activity of <scp>A</scp>shwagandha against human head and neck cancer cell lines

Lee, Haeng-Eun; Shin, Ji‐Ae; Jeong, Joseph H.; Jeon, Jongho; Cho, Sung‐Dae

doi:10.1111/jop.12353

Cited by 16 publications

(11 citation statements)

References 32 publications

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“…22,23 Our research group also reported that the methanol extract of Smilax china L. or b-phenylethyl isothiocyanate induced the DR5/caspase-8/Bid axis by regulating the extracellular signal-regulated kinase (ERK) or p38 MAPK signaling pathway, leading to caspase-mediated apoptosis in oral or cervical cancer cells. [24][25][26][27] These previous findings fully support DR5 regulation by natural products during apoptotic cell death pathways in cancer. In this study, our human apoptosis antibody array data showing that silymarin upregulates DR5 protein are consistent with these findings.…”

Section: Discussionsupporting

confidence: 73%

In vitro and in vivo anti-cancer activity of silymarin on oral cancer

et al. 2018

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Silymarin, a standardized extract from milk thistle fruits has been found to exhibit anti-cancer effects against various cancers. Here, we explored the anti-cancer activity of silymarin and its molecular target in human oral cancer in vitro and in vivo. Silymarin dose-dependently inhibited the proliferation of HSC-4 oral cancer cells and promoted caspase-dependent apoptosis. A human apoptosis protein array kit showed that death receptor 5 may be involved in silymarin-induced apoptosis, which was also shown through western blotting, immunocytochemistry, and reverse transcription-polymerase chain reaction. Silymarin increased cleaved caspase-8 and truncated Bid, leading to accumulation of cytochrome c. In addition, silymarin activated death receptor 5/caspase-8 to induce apoptotic cell death in two other oral cancer cell lines (YD15 and Ca9.22). Silymarin also suppressed tumor growth and volume without any hepatic or renal toxicity in vivo. Taken together, these results provide in vitro and in vivo evidence supporting the anti-cancer effect of silymarin and death receptor 5, and caspase-8 may be essential players in silymarin-mediated apoptosis in oral cancer.

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Section: Discussionsupporting

confidence: 73%

In vitro and in vivo anti-cancer activity of silymarin on oral cancer

et al. 2018

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“…It has also been found to selectively induce cell death in multiple types of tumor cells [143,144]. Its anticancer effects are mediated through modulation of a number of pathways, including inhibition of Notch 1 [145], inhibition of STAT3 activation [146–148], downregulation of the MTOR signalling components pS6K and p4E-BP1 [145], downregulation of the prosurvival pathway Akt/NF-kappaB/Bcl-2 [145], induction of c-Jun-NH(2)-kinase-mediated apoptosis [145], induction of apoptosis via upregulation of Bim, t-Bid, caspase-8, and DR5 [149], suppression of constitutive and IL-6-induced phosphorylation of STAT3 (on Tyr705) and consequent down-regulation of the STAT3 regulated genes Bcl-xL, Bcl-2, cyclin D1 and survivin [150], inhibition of heat shock protein 90 [151], downregulation of COX-2 and iNOS by blocking NF-κB activity [121], and down-regulation of TNF-a [152].…”

Section: Discussionmentioning

confidence: 99%

Towards natural mimetics of metformin and rapamycin

Aliper

Jellen

Cortese

et al. 2017

Aging

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Aging is now at the forefront of major challenges faced globally, creating an immediate need for safe, widescale interventions to reduce the burden of chronic disease and extend human healthspan. Metformin and rapamycin are two FDA-approved mTOR inhibitors proposed for this purpose, exhibiting significant anti-cancer and anti-aging properties beyond their current clinical applications. However, each faces issues with approval for off-label, prophylactic use due to adverse effects. Here, we initiate an effort to identify nutraceuticals—safer, naturally-occurring compounds—that mimic the anti-aging effects of metformin and rapamycin without adverse effects. We applied several bioinformatic approaches and deep learning methods to the Library of Integrated Network-based Cellular Signatures (LINCS) dataset to map the gene- and pathway-level signatures of metformin and rapamycin and screen for matches among over 800 natural compounds. We then predicted the safety of each compound with an ensemble of deep neural network classifiers. The analysis revealed many novel candidate metformin and rapamycin mimetics, including allantoin and ginsenoside (metformin), epigallocatechin gallate and isoliquiritigenin (rapamycin), and withaferin A (both). Four relatively unexplored compounds also scored well with rapamycin. This work revealed promising candidates for future experimental validation while demonstrating the applications of powerful screening methods for this and similar endeavors.

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“…Pretreatment with N -acetyl cysteine (NAC) or catalase abrogated withaferin-A-induced up-regulation of both CHOP and DR5 [ 68 ]. The induction of apoptosis in human head and neck carcinoma (MC3 and HN22) cells by withaferin-A was accompanied by upregulation of Bim, truncated Bid (t-Bid), cleavage of caspase-8, -3 and poly ADP ribose polymerase (PARP), and the elevated expression of DR5, suggesting an extrinsic pathway of apoptosis induction by this compound [ 67 ]. Mechanistically, the transcriptional activation of DR5 was mediated through withaferin-A-induced phosphorylation of ERK1/2 and ribosomal S6 kinase, and the induction of ETS-like transcription factor 1 (Elk1) and CHOP [ 78 ].…”

Section: Biochemical Basis Of Anticancer Effects Of Withaferin-amentioning

confidence: 99%

Withaferin-A—A Natural Anticancer Agent with Pleitropic Mechanisms of Action

Lee

Choi

2016

IJMS

131

107

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Cancer, being the second leading cause of mortality, exists as a formidable health challenge. In spite of our enormous efforts, the emerging complexities in the molecular nature of disease progression limit the real success in finding an effective cancer cure. It is now conceivable that cancer is, in fact, a progressive illness, and the morbidity and mortality from cancer can be reduced by interfering with various oncogenic signaling pathways. A wide variety of structurally diverse classes of bioactive phytochemicals have been shown to exert anticancer effects in a large number of preclinical studies. Multiple lines of evidence suggest that withaferin-A can prevent the development of cancers of various histotypes. Accumulating data from different rodent models and cell culture experiments have revealed that withaferin-A suppresses experimentally induced carcinogenesis, largely by virtue of its potent anti-oxidative, anti-inflammatory, anti-proliferative and apoptosis-inducing properties. Moreover, withaferin-A sensitizes resistant cancer cells to existing chemotherapeutic agents. The purpose of this review is to highlight the mechanistic aspects underlying anticancer effects of withaferin-A.

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Anticancer activity of Ashwagandha against human head and neck cancer cell lines

Abstract: These suggest that MEAG and WA may be potential natural materials for the treatment of HNSCC.

Cited by 16 publications

References 32 publications

In vitro and in vivo anti-cancer activity of silymarin on oral cancer

In vitro and in vivo anti-cancer activity of silymarin on oral cancer

Towards natural mimetics of metformin and rapamycin

Withaferin-A—A Natural Anticancer Agent with Pleitropic Mechanisms of Action

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