Proteomic analysis of β-asarone induced cytotoxicity in human glioblastoma U251 cells

Hu, Qi; Chen, Lu; Ning, Ling; Ma, Hui; Jiang, Zhuyun; Fu, Yue; Li, Li

doi:10.1016/j.jpba.2015.07.036

Cited by 19 publications

(19 citation statements)

References 28 publications

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“…Our recent investigation demonstrated that volatile oil of Acori tatarinowii Rhizoma (VOA) exhibited potent anti-tumor activity in glioma cells [ 14 ]. Moreover, we found that β-asarone ( Figure 1 A), the main component in the VOA, was shown to inhibit the growth of glioma cells [ 15 ], which was further confirmed by another group [ 16 ]. However, the inhibitory effect of β-asarone on the invasion and EMT of glioma cells remains unclear.…”

Section: Introductionsupporting

confidence: 60%

“…β-asarone, the major component in the VOA, has been shown to not only directly enter blood-brain barrier (BBB), but also improve the permeability of BBB and inhibit the function of P-glycoprotein [ 23 , 24 , 25 ]. Recent results from our group [ 15 ] and others [ 16 ] revealed that β-asarone effectively inhibited the growth of glioma cells. However, its effect on the invasion of glioma cells is still unknown.…”

Section: Discussionmentioning

confidence: 99%

“…However, the inhibitory effect of β-asarone on the invasion and EMT of glioma cells remains unclear. To comprehensively identify the potential molecular targets regulated by β-asarone, we applied a proteomic approach and identified hnRNP A2/B1 as one of the key protein targets [ 15 ]. It is interesting for us to further investigate the potential role of hnRNP A2/B1 in the anti-glioma effect of β-asarone.…”

Section: Introductionmentioning

confidence: 99%

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β-Asarone Inhibits Invasion and EMT in Human Glioma U251 Cells by Suppressing Splicing Factor HnRNP A2/B1

Wang

et al. 2018

Molecules

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β-asarone, the main component in the volatile oil of Acori tatarinowii Rhizoma, has been found to possess antitumor activity. However, its effect and mechanisms against tumor invasion and epithelial–mesenchymal transition (EMT) are still unclear. In this study, no or less cytotoxicity was caused by β-asarone within 0–120 μM in human glioma U251 cells for 48 h. β-asarone (30 and 60 μM) inhibited the migration of U251 cells in the wound healing assay, suppressed the invasion of U251 cells in the Boyden chamber invasion assay, and inhibited the adhesion of U251 cells onto the Matrigel. Moreover, β-asarone suppressed EMT with the up-regulation of E-cadherin and the down-regulation of vimentin. HnRNP A2/B1, a well-characterized oncogenic protein, was shown at a high basal level in U251 cells and β-asarone reduced hnRNP A2/B1 expression in a concentration and time-dependent way. Importantly, hnRNP A2/B1 overexpression significantly counteracted the inhibition of β-asarone on the migration, invasion, and adhesion of U251 cells and reversed the modulation of EMT markers by β-asarone. Additionally, β-asarone decreased the MMP-9 and p-STAT3 in U251 cells, which was also reversed by hnRNP A2/B1 overexpression. Together, our results suggest that hnRNP A2/B1 may be a potential molecular target underlying the inhibitory effect of β-asarone on invasion and EMT in glioma cells.

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Section: Introductionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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β-Asarone Inhibits Invasion and EMT in Human Glioma U251 Cells by Suppressing Splicing Factor HnRNP A2/B1

Wang

et al. 2018

Molecules

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“…Further, authors suggested that the hnRNP A2/B1 could be used as a biomarker for prediction of glioma progression and can act as a novel oncogene in glioblastoma. They concluded that (β)-asarone is effective as anti-tumor agent as it was shown to inhibit the expression of hnRNP H1, hnRNPA2/B1 and cathepsin D against brain tumor [21] .…”

Section: Main Textmentioning

confidence: 99%

“… Cell lines Treatment Targets/Possible molecular events Reference Glioblastoma (U251 cells) (β)-asarone (240 and 360 μM) Apoptosis (YO-PRO-1 and PI staining). Inhibition of the expression of hnRNP H1, hnRNPA2/B1 and cathepsin D. [21] Glioblastoma (U251 cells) (β)-asarone (30 and 60 μM) Inhibition of the migration (Wound healing assay). Suppression of the invasion (Boyden chamber invasion assay).…”

Section: Main Textmentioning

confidence: 99%

Experimental evidence for use of Acorus calamus (asarone) for cancer chemoprevention

Das

Swamy

Koti

et al. 2019

Heliyon

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Cancer is one of the major non-communicable diseases posing substantial challenges in both developing and developed countries. The options available for treatment of different cancer are associated with various limitations, including severe toxicity, drug resistance, poor outcomes and a high risk of relapse. Hence, an increased attention and necessity for screening of various phytochemicals from natural sources for superior and safer alternative has been ongoing for several decades. In recent years, phytochemicals like galantamine, erwinaze, rivastigmine, resveratrol from natural sources have been found to be important therapeutic targets for the treatment of various diseases including cancer, neurodegeneration, diabetes, and cardiovascular effects. Acorus calamus (Sweet flag), and/or its bioactive phytochemical alpha (α)-and beta (β)-asarone, is a well-known drug in the traditional system of medicine which possesses anti-tumor and chemo-preventive activities as evident from numerous pre-clinical studies both in-vitro and in-vivo . In this article, we critically review the current available scientific evidences of A. calamus and/or asarone for cancer chemoprevention based on preclinical in-vitro and in-vivo models. In addition, we also have compiled and discussed the molecular targets of mechanism(s) involved in the anti-cancer activity of A. calamus /asarone. Still, extensive in-vivo studies are necessary using various animal models to understand the molecular mechanism behind the pharmacological activity of the bioactive phytochemicals derived from A. calamus . It is strongly believed that the comprehensive evidence presented in this article could deliver a possible source for researchers to conduct future studies pertaining to A. calamus and/or its bioactive phytochemicals asarone for cancer chemoprevention.

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β‐asarone inhibits the migration, invasion, and EMT of bladder cancer through activating ER stress

Liu

Dan

et al. 2023

Cancer Medicine

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Background β‐asarone (β‐as), a compound extracted from Acorus calamus, has been found to have anticancer effects on a variety of human cancers. However, the potential effect of β‐as on bladder cancer (BCa) remains unknown. Methods After exposure to β‐as, migration, invasion, and epithelial‐mesenchymal transition (EMT) of BCa were determined by wound healing, transwell, and Western blot assays. Expression of proteins involved in the EMT and ER stress were explored by Western blot assays. Nude mouse xenograft model was served as the model system in vivo. Results The migration, invasion, and EMT of BCa were significantly inhibited after β‐as treatment. Further experiments revealed that endoplasmic reticulum (ER) stress is involved in β‐as‐mediated metastasis inhibition. In addition, β‐as significantly up‐regulated activating transcription factor 6 (ATF6), a branch of ER stress, and promoted its Golgi cleavage and nuclear localization. ATF6 silencing attenuated β‐as‐mediated metastasis and EMT inhibition in BCa cells. Conclusion Our data suggests that β‐as inhibits migration, invasion, and EMT of BCa by activating the ATF6 branch of ER stress. Thus, β‐as represents a potential candidate for BCa treatment.

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Proteomic analysis of β-asarone induced cytotoxicity in human glioblastoma U251 cells

Cited by 19 publications

References 28 publications

β-Asarone Inhibits Invasion and EMT in Human Glioma U251 Cells by Suppressing Splicing Factor HnRNP A2/B1

β-Asarone Inhibits Invasion and EMT in Human Glioma U251 Cells by Suppressing Splicing Factor HnRNP A2/B1

Experimental evidence for use of Acorus calamus (asarone) for cancer chemoprevention

β‐asarone inhibits the migration, invasion, and EMT of bladder cancer through activating ER stress

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