Kurarinone Synergizes TRAIL-Induced Apoptosis in Gastric Cancer Cells

Zhou, Wenchao; A, Cao; Wang, Li; Wu, Di

doi:10.1007/s12013-014-0444-0

Cited by 22 publications

(16 citation statements)

References 46 publications

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“…Second, resistant mechanism of TRAIL-induced apoptosis is disrupted through downregulation of cFLIP expression. Natural compounds such as kurarinone (20), icaritin (21), withanolide E (22) were reported to downregulate cFLIP expression and subsequent sensitization of TRAIL-resistant cancer cells to TRAIL-induced apoptosis. Natural compounds, such as silibinin (23), gingerol (24) and indomethacin (25) were reported to possess both mechanisms of sensitizing TRAIL-resistant cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Goniothalamin enhances TRAIL-induced apoptosis in colorectal cancer cells through DR5 upregulation and cFLIP downregulation

Sophonnithiprasert

Nilwarangkoon

Nakamura

et al. 2015

International Journal of Oncology

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Abstract. The combination of TNF-related apoptosis-inducing ligand (TRAIL) and bioactive compound to enhance apoptosis in TRAIL-resistant cancer is one of cancer treatment strategies. TRAIL possesses the unique capacity to selectively induce apoptosis in cancer cells both in vitro and in vivo with little effect on normal cells. Recent studies have reported that there are many TRAIL-resistant cancers. Thus, bioactive compounds that enhance cytotoxicity of TRAIL would be potential candidates for cancer therapeutic application. This study evaluated the cytotoxic and apoptosis induction upon combined treatment of TRAIL and goniothalamin, the natural styryl-lactone compound extracted from plant Goniothalamus spp., in LoVo cells. The results showed that a combination of goniothalamin and TRAIL enhanced caspase-dependent apoptosis induction in LoVo cells via both death receptor-and mitochondrial-mediated apoptosis pathways. In addition, goniothalamin enhanced TRAIL-induced apoptosis through increased death receptor DR5 expression and decreased anti-apoptotic regulator cFLIP. Interestingly, goniothalamin increased translocation of DR5 to cell surface and consequently contributed to the enhancement of TRAIL-induced apoptosis. In conclusion, this is the first report showing the combined treatment of goniothalamin and TRAIL was able to effectively enhance TRAIL-mediated apoptosis induction in TRAIL-refractory colorectal cancer, LoVo cells. Therefore, this study may offer a strategic cancer treatment against TRAIL-resistant cancers.

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Section: Introductionmentioning

confidence: 99%

Goniothalamin enhances TRAIL-induced apoptosis in colorectal cancer cells through DR5 upregulation and cFLIP downregulation

Sophonnithiprasert

Nilwarangkoon

Nakamura

et al. 2015

International Journal of Oncology

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“…Additionally, some of the agents that their combined using with TRAIL has been acceptable outcomes but in limited cell lines have been listed below. kurarinone (Seo et al, ; Zhou, Cao, Wang, & Wu, ), monensin (Yoon et al, ), paxiline (Kang et al, ), diclofenac/hyaluronic acid (Dic/HA) (Fecker et al, ), nickel2+ (Schmidt et al, ), SHetA2 (Lin et al, ), BAY 11–7085 (Shen et al, ), compound c (Jang et al, ), FAK inhibitor PH11 (Dao et al, ), caffeic acid phenethyl ester (CAPE) (Li, Wu, et al, ), fasudil (Wang et al, ), cathepsin S inhibitor ZFL (Seo et al, ), 4‐(4‐Chloro‐2‐methylphenoxy)‐N‐hydroxybutanamide (CMH) (Bijangi‐Vishehsaraei, Huang, Safa, Saadatzadeh, & Murphy, ), actinomycin (Haimerl, Erhardt, Sass, & Tiegs, ), H1 (derivative of tetrandrine) (Lin, Wang, et al, ), genistein (Siegelin, Siegelin, Habel, & Gaiser, ), icaritin (Han, Xu, et al, ), ABT‐737 and VX–680 (Choi et al, ), 6‐shogaol (Han, Woo, et al, ), cathepsin E (Yasukochi, Kawakubo, Nakamura, & Yamamoto, ), ozarelix (Festuccia et al, ), transglutaminase 2 inhibitor (TGM2I) (Li, Xu, Bai, Chen, & Lin, ), amurensin G (Kim, Kim, Lee, et al, ), volasertib (Jeon et al, ), temozolomide (TMZ) (Zhitao, Long, Jia, Yunchao, & Anhua, ), chalcone‐24 (Xu et al, ), gingerol (Lee, Kim, Jung, Lee, & Park, ), triptolide (Chen et al, ), AKT inhibitor API‐1 (Li, Ren, et al, ), smac mimetic compounds (SMC) (Cheung et al, ), dicoumarol (Park, Min, Choi, & Kwon, ), partenolide (Trang et al, ), Pyrrolo‐1, 5‐benzoxazepine (PBOX) (Nathwani et al, ), embelin (Siegelin, Gaiser, & Siegelin, ), myricetin (Siegelin, Gaiser, Habel, & Siegelin, ), quercetin (Jung, Heo, Lee, Kwon, & Kim, ), silibinin (Son et al, ), epigallocatechin gallate (EGCG) (Abou El Naga et al, ), icariside II (Du et al, ), anisomycin (Seo et al, ), dioscin (Kim, Kim, Park, et al, ), celecoxib (Chen et al, ), micro RNA 126 (MiR‐126) (Zhang, Zhou, Zhu, & Yuan, ), gambognic acid (Ye et al, ), survivin inhibitor YM155 (Woo, Min, Seo, &...…”

Section: Intracellular Anti‐apoptotic Proteins As Targeted Therapymentioning

confidence: 99%

Down‐regulation of intracellular anti‐apoptotic proteins, particularly c‐FLIP by therapeutic agents; the novel view to overcome resistance to TRAIL

Hassanzadeh

Hagh

Alivand

et al. 2018

Journal Cellular Physiology

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL or Apo2L) is a member of the tumor necrosis factor (TNF) superfamily that induces apoptosis in different types of cancer cells via activation of caspase cascade. TRAIL interacts with its cognate receptors that placed on cancer cells surface, including TRAIL-R1 (death receptor 4, DR4), TRAIL-R2 (death receptor 5, DR5), TRAIL-R3 (decoy receptor 1, DcR1), TRAIL-R4 (decoy receptor 2, DcR2), and osteoprotegerin (OPG). Despite high apoptosis-inducing ability of TRAIL, various cancerous cells gain resistance to TRAIL gradually, and consequently TRAIL potential for apoptosis stimulation in these cells diminishes intensely. According to diverse ranges of examinations, intracellular anti-apoptotic proteins, such as cellular-FLICE inhibitory protein (c-FLIP), apoptosis inhibitors (IAPs), myeloid cell leukemia sequence 1 (MCL-1), BCL-2, BCL-XL, and survivin play key role in cancer cells resistance to TRAIL. These proteins attenuate cancer cells sensitivity to TRAIL via various functions, importantly through caspase cascade suppression. The c-FLIP avoids from caspase 8 activation by FADD via binding to caspase 8 cleavage of FADD. Moreover, it activates signaling pathways that involved in cancer cells survival and proliferation. Intriguingly, it appears that the down-regulation of intracellular anti-apoptotic proteins, particularly c-FLIP is effectiveness goal for TRAIL-resistant cancers therapy, because their up-regulation in association with poor prognosis has been observed in various types of TRAIL-resistant cancers. In this review, we tried to collect and examine investigations that researchers have been able to sensitize cancer cells to TRAIL through targeting of c-FLIP alone or with other intracellular anti-apoptotic proteins directly or indirectly. It seems that co-treatment of resistant cells by TRAIL with other therapeutic agents with the aim of intracellular anti-apoptotic proteins inhibition is hopeful and attractive approach to overcome various TRAIL-resistant cancers.

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“…Kurarinone is one of prenylated flavonones isolated from the roots of Sophora flavescens . Pharmacological study suggested that kurarinone exhibited estrogenic (De Naeyer et al, 2004), anti‐microbial (Chen et al, 2005), anti‐cancer (Xie et al, 2018; Yang et al, 2018; Zhou, Cao, Wang, & Wu, 2015), anti‐virus (Pan, Yu, Yan, & Zhang, 2005) activities. Kurarinone possessed urinary bladder‐relaxant effect depending on the potentiation of large‐conductance Ca 2+ ‐activated K + channels (Lee et al, 2016) and immune regulation effects (Kim et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Pharmacokinetic and bioavailability study of kurarinone in dog plasma by UHPLC–MS/MS

Huang

Lin

Chen

et al. 2020

Biomedical Chromatography

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Kurarinone, a natural prenylated flavonone isolated from Sophora flavescens, has been exhibited various activities. This study aimed to establish a simple and sensitive ultrahigh performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) method for determining kurarinone in dog plasma. Acetonitrile-mediated precipitation was applied for sample pretreatment. Chromatographic separation was achieved on a Waters ACQUITY HSS T3 (100 × 2.1 mm, i. d., 1.8 μm) column with gradient elution using water containing 0.1% formic acid and acetonitrile as mobile phase. Quantitation was performed using an electrospray ionization source in negative multiple reaction monitoring mode. The linearity of this method was over the concentration range 0.1-500 ng/mL with the lowest limit of quantification (LLOQ) of 0.1 ng/mL. The intra-and inter-day precision was less than 10.51% and the accuracy ranged from 94.85% to 97.72%, respectively. The extraction recovery of kurarinone in dog plasma was more than 82.37% and no significant matrix effect was observed. The analyte was stable under tested storage conditions. The validated method was further successfully applied to a preclinical pharmacokinetic study of kurarinone in dog after a single intravenous (2 mg/kg) and oral (20 mg/kg) administration. The results revealed that kurarinone was rapidly absorbed into plasma with good bioavailability (38.19%) and low clearance.

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Kurarinone Synergizes TRAIL-Induced Apoptosis in Gastric Cancer Cells

Cited by 22 publications

References 46 publications

Goniothalamin enhances TRAIL-induced apoptosis in colorectal cancer cells through DR5 upregulation and cFLIP downregulation

Goniothalamin enhances TRAIL-induced apoptosis in colorectal cancer cells through DR5 upregulation and cFLIP downregulation

Down‐regulation of intracellular anti‐apoptotic proteins, particularly c‐FLIP by therapeutic agents; the novel view to overcome resistance to TRAIL

Pharmacokinetic and bioavailability study of kurarinone in dog plasma by UHPLC–MS/MS

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