The Experts below are selected from a list of 2094 Experts worldwide ranked by ideXlab platform
Zhi-jun Zhang - One of the best experts on this subject based on the ideXlab platform.
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Ligustilide ameliorates inflammatory pain and inhibits tlr4 upregulation in spinal astrocytes following complete freund s adjuvant peripheral injection
Cellular and Molecular Neurobiology, 2016Co-Authors: Bin Qian, Lin-xia Zhao, Yong-jing Gao, Yu-lin Dong, Zhi-jun ZhangAbstract:Ligustilide is a major component of Radix Angelica Sinensis and reported to have anti-inflammatory and anti-nociceptive effects. Toll-like receptor 4 (TLR4) has been shown to be expressed in the spinal cord and be involved in inflammatory pain and neuropathic pain. Whether Ligustilide can inhibit spinal TLR4 expression in inflammatory pain is still unknown. In the present study, we intravenously injected Ligustilide daily for 4 days, with the first injection given at 1 h before complete Freund’s adjuvant (CFA) injection. We tested the analgesic effect of Ligustilide by behavioral test and checked the expression and distribution of TLR4 in the spinal cord by real-time quantitative PCR, Western blot, and immunofluorescence. Our data showed that repeated daily intravenous treatment with Ligustilide alleviated CFA-induced heat hyperalgesia and mechanical allodynia. The same treatment also inhibited CFA-induced TLR4 mRNA and protein increase in the spinal cord. Immunofluorescence double staining showed that TLR4 was predominantly expressed in spinal astrocytes. In primary cultured astrocytes, Ligustilide dose-dependently reduced lipopolysaccharide-induced upregulation of TLR4 mRNA expression. These data indicate that Ligustilide treatment reduces TLR4 expression in spinal astrocytes and is an effective therapy for inflammatory pain.
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Ligustilide Ameliorates Inflammatory Pain and Inhibits TLR4 Upregulation in Spinal Astrocytes Following Complete Freund’s Adjuvant Peripheral Injection
Cellular and molecular neurobiology, 2015Co-Authors: Bin Qian, Lin-xia Zhao, Yong-jing Gao, Yu-lin Dong, Zhi-jun ZhangAbstract:Ligustilide is a major component of Radix Angelica Sinensis and reported to have anti-inflammatory and anti-nociceptive effects. Toll-like receptor 4 (TLR4) has been shown to be expressed in the spinal cord and be involved in inflammatory pain and neuropathic pain. Whether Ligustilide can inhibit spinal TLR4 expression in inflammatory pain is still unknown. In the present study, we intravenously injected Ligustilide daily for 4 days, with the first injection given at 1 h before complete Freund’s adjuvant (CFA) injection. We tested the analgesic effect of Ligustilide by behavioral test and checked the expression and distribution of TLR4 in the spinal cord by real-time quantitative PCR, Western blot, and immunofluorescence. Our data showed that repeated daily intravenous treatment with Ligustilide alleviated CFA-induced heat hyperalgesia and mechanical allodynia. The same treatment also inhibited CFA-induced TLR4 mRNA and protein increase in the spinal cord. Immunofluorescence double staining showed that TLR4 was predominantly expressed in spinal astrocytes. In primary cultured astrocytes, Ligustilide dose-dependently reduced lipopolysaccharide-induced upregulation of TLR4 mRNA expression. These data indicate that Ligustilide treatment reduces TLR4 expression in spinal astrocytes and is an effective therapy for inflammatory pain.
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Ligustilide inhibits microglia-mediated proinflammatory cytokines production and inflammatory pain.
Brain research bulletin, 2014Co-Authors: Ming-di Zhu, Lin-xia Zhao, Xiao-tian Wang, Yong-jing Gao, Zhi-jun ZhangAbstract:Ligustilide is the main component of Danggui essential oil, and recently reported to have anti-inflammatory and neuroprotective effect. Increasing evidence suggests that glia-mediated neuroinflammation in the spinal cord plays a vital role in the pathogenesis of chronic pain. In the present study, we investigated the anti-inflammatory and anti-nociceptive effect of Ligustilide both in vitro and in vivo. In microglial cell line BV2 cells, lipopolysaccharide (LPS) time-dependently increased the mRNA expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6), which was decreased by pretreatment with Ligustilide in a dose-dependent manner. Ligustilide also decreased LPS-induced proinflammatory cytokines production in primary cultured microglia. In vivo, intrathecal injection of LPS induced mechanical allodynia in mice. Intravenous injection of Ligustilide prevented LPS-induced mechanical allodynia, and decreased LPS-induced TNF-α, IL-1β, and IL-6 up-regulation in the spinal cord. In addition, repetitive intravenous injection of Ligustilide attenuated intraplantar injection of complete Freund's adjuvant (CFA)-induced mechanical allodynia and thermal hyperalgesia. The same treatment of Ligustilide also inhibited CFA-induced TNF-α, IL-1β, and IL-6 up-regulation and microglial activation in the spinal cord. Taken together, our data suggest that Ligustilide can alleviate inflammatory pain partly through inhibition of microglial activation and proinflammatory cytokines production, which indicates a possible benefit from the use of Ligustilide in the treatment of inflammatory pain and neuroinflammation-associated disorders.
Hong Yang - One of the best experts on this subject based on the ideXlab platform.
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Ligustilide inhibits vascular smooth muscle cells proliferation.
European journal of pharmacology, 2006Co-Authors: Tai-qiu Qiu, Hong YangAbstract:Proliferation and migration of vascular smooth muscle cells (VSMCs) are believed to develop atherosclerosis and venous bypass graft disease. Ligustilide is widely used to treat some pathological settings such as atherosclerosis and hypertension. The aim of this study was to examine the effect of Ligustilide on VSMCs proliferation. The results show that Ligustilide significantly inhibited VSMCs proliferation and cell cycle progression. Further analysis shows that Ligustilide suppressed reactive oxygen species production and extracellular signal-related kinases (ERK), c-Jun N-terminal protein kinase (JNK), and p38 MAP kinase. Cells were treated with antioxidant, superoxide dismutase, catalase, and DPI, respectively, leading to repress ERK, JNK, and p38 activation. The inhibitors of mitogen activated protein kinase (MAPK), PD98059, SB203580, and Sp600125, inhibited cell proliferation. These findings suggest the antiproliferative effect of Ligustilide was associated with the decrement of reactive oxygen species resulting in the suppression of MAPK pathway. Thus, Ligustilide contribute to be the effective agent in preventing cardiovascular diseases.
Chengqiang Wang - One of the best experts on this subject based on the ideXlab platform.
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Z-Ligustilide Exerted Hormetic Effect on Growth and Detoxification Enzymes of Spodoptera litura Larvae
Evidence-based complementary and alternative medicine : eCAM, 2018Co-Authors: Guojun Dou, Chengqiang Wang, Jia Zhou, Dejun Liu, Jianyou ShiAbstract:Plants have evolved a variety of phytochemicals to defense insect feeding, whereas insects have also evolved diverse detoxification enzymes, which are adaptively induced as a prosurvival mechanism. Herein, Z-Ligustilide in Ligusticum chuanxiong Hort. was found to exhibit a similar trend in the accumulation from December to May as the occurrence of Spodoptera litura (Fabricius) larvae. Importantly, S. litura larvae feeding enhanced Z-Ligustilide level in the stem and leaf (p levistilide A > senkyunolide A > 3-butylidenephthalide > senkyunolide I, implicating the critical role of conjugated structure. Notably, there was a biphasic dose response for glutathione S-transferase (GST), cytochrome P450 (CYP) 450, Acetylcholinesterase (AChE), and Carboxylesterase (CarE) activities and GSTs1, cytochrome P450 (CYP) 4S9, and CYP4M14 mRNA expression. Particularly, low dose (0.1 mg·g−1) of Z-Ligustilide conferred the resistance of S. litura larvae against chlorpyrifos (p < 0.05). Together, our data suggest that Z-Ligustilide may function in a hormetic way in the chemical defense of L. chuanxiong against S. litura larvae.
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Z-Ligustilide Exerted Hormetic Effect on Growth and Detoxification Enzymes of Spodoptera litura Larvae
Hindawi Limited, 2018Co-Authors: Guojun Dou, Chengqiang Wang, Jia Zhou, Dejun Liu, Jianyou ShiAbstract:Plants have evolved a variety of phytochemicals to defense insect feeding, whereas insects have also evolved diverse detoxification enzymes, which are adaptively induced as a prosurvival mechanism. Herein, Z-Ligustilide in Ligusticum chuanxiong Hort. was found to exhibit a similar trend in the accumulation from December to May as the occurrence of Spodoptera litura (Fabricius) larvae. Importantly, S. litura larvae feeding enhanced Z-Ligustilide level in the stem and leaf (p < 0.01). Moreover, Z-Ligustilide ranging from 1 to 5 mg·g−1 exhibited remarkable larvicidal activity, antifeedant activity, and growth inhibition against S. litura larvae. The LC50 values of larvicidal activity for phthalides in L. chuanxiong were compared as follows: Z-Ligustilide > levistilide A > senkyunolide A > 3-butylidenephthalide > senkyunolide I, implicating the critical role of conjugated structure. Notably, there was a biphasic dose response for glutathione S-transferase (GST), cytochrome P450 (CYP) 450, Acetylcholinesterase (AChE), and Carboxylesterase (CarE) activities and GSTs1, cytochrome P450 (CYP) 4S9, and CYP4M14 mRNA expression. Particularly, low dose (0.1 mg·g−1) of Z-Ligustilide conferred the resistance of S. litura larvae against chlorpyrifos (p < 0.05). Together, our data suggest that Z-Ligustilide may function in a hormetic way in the chemical defense of L. chuanxiong against S. litura larvae
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sensitization of tamoxifen resistant breast cancer cells by z Ligustilide through inhibiting autophagy and accumulating dna damages
Oncotarget, 2017Co-Authors: Zhuyun Jiang, Chengqiang Wang, Yi YangAbstract:// Hongyi Qi 1, * , Zhuyun Jiang 1, * , Chengqiang Wang 1 , Yi Yang 1 , Li Li 1 , Hui He 1 , Zanyang Yu 1 1 College of Pharmaceutical Sciences, Southwest University, Beibei District, Chongqing 400716, China * These authors have contributed equally to this work Correspondence to: Hongyi Qi, email: hongyiqi@swu.edu.cn Keywords: Z-Ligustilide, tamoxifen, autophagic flux, chemoresistance, DNA damage Received: February 21, 2017 Accepted: March 26, 2017 Published: April 04, 2017 ABSTRACT Autophagy plays a pro-survival role in the tamoxifen-resistant breast cancer cells. Herein we found that autophagy was concomitantly induced in tamoxifen-resistant MCF-7 (MCF-7 TR5 ) cells through the dissociation of Bcl-2 from Beclin 1 and subsequent enhancement of interaction among the ATG14-Beclin1-PI3KC3 complex. Moreover, higher level of DNA damage was observed in MCF-7 TR5 cells with the decreased BRCA1 and RAD51 level and the increased Ku80 level. Interestingly, Nur77 was selectively degraded by autophagy, which causes the release of Ku80 from the Nur77-Ku80 complex, resulting in the increase of the DNA binding of Ku80 and DNA-PKcs. Meanwhile, Z-Ligustilide, a phthalide compound from Radix Angelica sinensis , was shown to inhibit the autophagic flux by blocking the autophagosome-lysosome fusion. Importantly, Z-Ligustilide-mediated autophagy inhibition restored Nur77 expression in MCF-7 TR5 cells. Furthermore, Z-Ligustilide promoted the interaction of Nur77 with Ku80 and thereby abolished the association of DNA-PKcs with DNA ends. Moreover, Z-Ligustilide sensitized MCF-7 TR5 cells in a caspase-independent cell death and enhanced the DNA damage caused by tamoxifen, which was found to be attenuated by shNur77. Together, these findings not only provide important insights into the formation of tamoxifen resistance in breast cancer cells, but also suggest Z-Ligustilide may function as a novel autophagy inhibitor to overcome chemoresistance.
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z Ligustilide restores tamoxifen sensitivity of era negative breast cancer cells by reversing mta1 ifi16 hdacs complex mediated epigenetic repression of era
Oncotarget, 2017Co-Authors: Guojun Dou, Chengqiang WangAbstract:// Hui Ma 1, * , Li Li 1, * , Guojun Dou 1 , Chengqiang Wang 1 , Juan Li 1 , Hui He 1 , Mingxia Wu 1 and Hongyi Qi 1 1 College of Pharmaceutical Sciences, Southwest University, Chongqing 400716, China * These authors have contributed equally to this work Correspondence to: Hongyi Qi, email: hongyiqi@swu.edu.cn Keywords: Z-Ligustilide, tamoxifen, ERα negative breast cancer, MTA1, histone modification Received: January 13, 2017 Accepted: March 02, 2017 Published: March 22, 2017 ABSTRACT Emerging evidence indicates epigenetic modification represses estrogen receptor α (ERα) and contributes to the resistance to tamoxifen in aggressive ERα-negative (ERα - ) breast cancer. Z-Ligustilide is a major compound in Radix Angelica sinensis , an herb from traditional Chinese medicine (TCM) most frequently prescribed for breast cancer. However, the role of Z-Ligustilide in ERα - breast cancer and epigenetic modification remains largely unknown. Herein we showed, for the first time, that Z-Ligustilide restored the growth inhibition of tamoxifen on ERα - breast cancer cells. Apoptosis and S and G2/M phases cell cycle arrest were induced by combinatorial Z-Ligustilide and tamoxifen. Importantly, Z-Ligustilide reactivated the ERα expression and transcriptional activity, which is proved to be indispensable for restoring the sensitivity to tamoxifen. Interestingly, Z-Ligustilide increased Ace-H3 (lys9/14) enrichment in the ERα promoter. Moreover, Z-Ligustilide dramatically reduced the enrichment of metastasis-associated protein 1 (MTA1) as well as IFN-γ-inducible protein 16 (IFI16) and histone deacetylases (HDACs) onto the ERα promoter. Meanwhile, Z-Ligustilide downregulated MTA1, IFI16 and HDACs, which caused destabilization of the corepressor complex. Collectively, our study not only highlights Z-Ligustilide as a novel epigenetic modulator, but also opens new possibilities from TCM for treating aggressive tamoxifen-resistant breast cancer.
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Z-Ligustilide restores tamoxifen sensitivity of ERa negative breast cancer cells by reversing MTA1/IFI16/HDACs complex mediated epigenetic repression of ERa.
Oncotarget, 2017Co-Authors: Guojun Dou, Chengqiang WangAbstract:// Hui Ma 1, * , Li Li 1, * , Guojun Dou 1 , Chengqiang Wang 1 , Juan Li 1 , Hui He 1 , Mingxia Wu 1 and Hongyi Qi 1 1 College of Pharmaceutical Sciences, Southwest University, Chongqing 400716, China * These authors have contributed equally to this work Correspondence to: Hongyi Qi, email: hongyiqi@swu.edu.cn Keywords: Z-Ligustilide, tamoxifen, ERα negative breast cancer, MTA1, histone modification Received: January 13, 2017 Accepted: March 02, 2017 Published: March 22, 2017 ABSTRACT Emerging evidence indicates epigenetic modification represses estrogen receptor α (ERα) and contributes to the resistance to tamoxifen in aggressive ERα-negative (ERα - ) breast cancer. Z-Ligustilide is a major compound in Radix Angelica sinensis , an herb from traditional Chinese medicine (TCM) most frequently prescribed for breast cancer. However, the role of Z-Ligustilide in ERα - breast cancer and epigenetic modification remains largely unknown. Herein we showed, for the first time, that Z-Ligustilide restored the growth inhibition of tamoxifen on ERα - breast cancer cells. Apoptosis and S and G2/M phases cell cycle arrest were induced by combinatorial Z-Ligustilide and tamoxifen. Importantly, Z-Ligustilide reactivated the ERα expression and transcriptional activity, which is proved to be indispensable for restoring the sensitivity to tamoxifen. Interestingly, Z-Ligustilide increased Ace-H3 (lys9/14) enrichment in the ERα promoter. Moreover, Z-Ligustilide dramatically reduced the enrichment of metastasis-associated protein 1 (MTA1) as well as IFN-γ-inducible protein 16 (IFI16) and histone deacetylases (HDACs) onto the ERα promoter. Meanwhile, Z-Ligustilide downregulated MTA1, IFI16 and HDACs, which caused destabilization of the corepressor complex. Collectively, our study not only highlights Z-Ligustilide as a novel epigenetic modulator, but also opens new possibilities from TCM for treating aggressive tamoxifen-resistant breast cancer.
Tai-qiu Qiu - One of the best experts on this subject based on the ideXlab platform.
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Ligustilide inhibits vascular smooth muscle cells proliferation.
European journal of pharmacology, 2006Co-Authors: Tai-qiu Qiu, Hong YangAbstract:Proliferation and migration of vascular smooth muscle cells (VSMCs) are believed to develop atherosclerosis and venous bypass graft disease. Ligustilide is widely used to treat some pathological settings such as atherosclerosis and hypertension. The aim of this study was to examine the effect of Ligustilide on VSMCs proliferation. The results show that Ligustilide significantly inhibited VSMCs proliferation and cell cycle progression. Further analysis shows that Ligustilide suppressed reactive oxygen species production and extracellular signal-related kinases (ERK), c-Jun N-terminal protein kinase (JNK), and p38 MAP kinase. Cells were treated with antioxidant, superoxide dismutase, catalase, and DPI, respectively, leading to repress ERK, JNK, and p38 activation. The inhibitors of mitogen activated protein kinase (MAPK), PD98059, SB203580, and Sp600125, inhibited cell proliferation. These findings suggest the antiproliferative effect of Ligustilide was associated with the decrement of reactive oxygen species resulting in the suppression of MAPK pathway. Thus, Ligustilide contribute to be the effective agent in preventing cardiovascular diseases.
Guojun Dou - One of the best experts on this subject based on the ideXlab platform.
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Z-Ligustilide Exerted Hormetic Effect on Growth and Detoxification Enzymes of Spodoptera litura Larvae
Evidence-based complementary and alternative medicine : eCAM, 2018Co-Authors: Guojun Dou, Chengqiang Wang, Jia Zhou, Dejun Liu, Jianyou ShiAbstract:Plants have evolved a variety of phytochemicals to defense insect feeding, whereas insects have also evolved diverse detoxification enzymes, which are adaptively induced as a prosurvival mechanism. Herein, Z-Ligustilide in Ligusticum chuanxiong Hort. was found to exhibit a similar trend in the accumulation from December to May as the occurrence of Spodoptera litura (Fabricius) larvae. Importantly, S. litura larvae feeding enhanced Z-Ligustilide level in the stem and leaf (p levistilide A > senkyunolide A > 3-butylidenephthalide > senkyunolide I, implicating the critical role of conjugated structure. Notably, there was a biphasic dose response for glutathione S-transferase (GST), cytochrome P450 (CYP) 450, Acetylcholinesterase (AChE), and Carboxylesterase (CarE) activities and GSTs1, cytochrome P450 (CYP) 4S9, and CYP4M14 mRNA expression. Particularly, low dose (0.1 mg·g−1) of Z-Ligustilide conferred the resistance of S. litura larvae against chlorpyrifos (p < 0.05). Together, our data suggest that Z-Ligustilide may function in a hormetic way in the chemical defense of L. chuanxiong against S. litura larvae.
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Z-Ligustilide Exerted Hormetic Effect on Growth and Detoxification Enzymes of Spodoptera litura Larvae
Hindawi Limited, 2018Co-Authors: Guojun Dou, Chengqiang Wang, Jia Zhou, Dejun Liu, Jianyou ShiAbstract:Plants have evolved a variety of phytochemicals to defense insect feeding, whereas insects have also evolved diverse detoxification enzymes, which are adaptively induced as a prosurvival mechanism. Herein, Z-Ligustilide in Ligusticum chuanxiong Hort. was found to exhibit a similar trend in the accumulation from December to May as the occurrence of Spodoptera litura (Fabricius) larvae. Importantly, S. litura larvae feeding enhanced Z-Ligustilide level in the stem and leaf (p < 0.01). Moreover, Z-Ligustilide ranging from 1 to 5 mg·g−1 exhibited remarkable larvicidal activity, antifeedant activity, and growth inhibition against S. litura larvae. The LC50 values of larvicidal activity for phthalides in L. chuanxiong were compared as follows: Z-Ligustilide > levistilide A > senkyunolide A > 3-butylidenephthalide > senkyunolide I, implicating the critical role of conjugated structure. Notably, there was a biphasic dose response for glutathione S-transferase (GST), cytochrome P450 (CYP) 450, Acetylcholinesterase (AChE), and Carboxylesterase (CarE) activities and GSTs1, cytochrome P450 (CYP) 4S9, and CYP4M14 mRNA expression. Particularly, low dose (0.1 mg·g−1) of Z-Ligustilide conferred the resistance of S. litura larvae against chlorpyrifos (p < 0.05). Together, our data suggest that Z-Ligustilide may function in a hormetic way in the chemical defense of L. chuanxiong against S. litura larvae
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z Ligustilide restores tamoxifen sensitivity of era negative breast cancer cells by reversing mta1 ifi16 hdacs complex mediated epigenetic repression of era
Oncotarget, 2017Co-Authors: Guojun Dou, Chengqiang WangAbstract:// Hui Ma 1, * , Li Li 1, * , Guojun Dou 1 , Chengqiang Wang 1 , Juan Li 1 , Hui He 1 , Mingxia Wu 1 and Hongyi Qi 1 1 College of Pharmaceutical Sciences, Southwest University, Chongqing 400716, China * These authors have contributed equally to this work Correspondence to: Hongyi Qi, email: hongyiqi@swu.edu.cn Keywords: Z-Ligustilide, tamoxifen, ERα negative breast cancer, MTA1, histone modification Received: January 13, 2017 Accepted: March 02, 2017 Published: March 22, 2017 ABSTRACT Emerging evidence indicates epigenetic modification represses estrogen receptor α (ERα) and contributes to the resistance to tamoxifen in aggressive ERα-negative (ERα - ) breast cancer. Z-Ligustilide is a major compound in Radix Angelica sinensis , an herb from traditional Chinese medicine (TCM) most frequently prescribed for breast cancer. However, the role of Z-Ligustilide in ERα - breast cancer and epigenetic modification remains largely unknown. Herein we showed, for the first time, that Z-Ligustilide restored the growth inhibition of tamoxifen on ERα - breast cancer cells. Apoptosis and S and G2/M phases cell cycle arrest were induced by combinatorial Z-Ligustilide and tamoxifen. Importantly, Z-Ligustilide reactivated the ERα expression and transcriptional activity, which is proved to be indispensable for restoring the sensitivity to tamoxifen. Interestingly, Z-Ligustilide increased Ace-H3 (lys9/14) enrichment in the ERα promoter. Moreover, Z-Ligustilide dramatically reduced the enrichment of metastasis-associated protein 1 (MTA1) as well as IFN-γ-inducible protein 16 (IFI16) and histone deacetylases (HDACs) onto the ERα promoter. Meanwhile, Z-Ligustilide downregulated MTA1, IFI16 and HDACs, which caused destabilization of the corepressor complex. Collectively, our study not only highlights Z-Ligustilide as a novel epigenetic modulator, but also opens new possibilities from TCM for treating aggressive tamoxifen-resistant breast cancer.
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Z-Ligustilide restores tamoxifen sensitivity of ERa negative breast cancer cells by reversing MTA1/IFI16/HDACs complex mediated epigenetic repression of ERa.
Oncotarget, 2017Co-Authors: Guojun Dou, Chengqiang WangAbstract:// Hui Ma 1, * , Li Li 1, * , Guojun Dou 1 , Chengqiang Wang 1 , Juan Li 1 , Hui He 1 , Mingxia Wu 1 and Hongyi Qi 1 1 College of Pharmaceutical Sciences, Southwest University, Chongqing 400716, China * These authors have contributed equally to this work Correspondence to: Hongyi Qi, email: hongyiqi@swu.edu.cn Keywords: Z-Ligustilide, tamoxifen, ERα negative breast cancer, MTA1, histone modification Received: January 13, 2017 Accepted: March 02, 2017 Published: March 22, 2017 ABSTRACT Emerging evidence indicates epigenetic modification represses estrogen receptor α (ERα) and contributes to the resistance to tamoxifen in aggressive ERα-negative (ERα - ) breast cancer. Z-Ligustilide is a major compound in Radix Angelica sinensis , an herb from traditional Chinese medicine (TCM) most frequently prescribed for breast cancer. However, the role of Z-Ligustilide in ERα - breast cancer and epigenetic modification remains largely unknown. Herein we showed, for the first time, that Z-Ligustilide restored the growth inhibition of tamoxifen on ERα - breast cancer cells. Apoptosis and S and G2/M phases cell cycle arrest were induced by combinatorial Z-Ligustilide and tamoxifen. Importantly, Z-Ligustilide reactivated the ERα expression and transcriptional activity, which is proved to be indispensable for restoring the sensitivity to tamoxifen. Interestingly, Z-Ligustilide increased Ace-H3 (lys9/14) enrichment in the ERα promoter. Moreover, Z-Ligustilide dramatically reduced the enrichment of metastasis-associated protein 1 (MTA1) as well as IFN-γ-inducible protein 16 (IFI16) and histone deacetylases (HDACs) onto the ERα promoter. Meanwhile, Z-Ligustilide downregulated MTA1, IFI16 and HDACs, which caused destabilization of the corepressor complex. Collectively, our study not only highlights Z-Ligustilide as a novel epigenetic modulator, but also opens new possibilities from TCM for treating aggressive tamoxifen-resistant breast cancer.