The anti-herpetic activity of trichosanthin via the nuclear factor-κB and p53 pathways

He, Dongxu; Zheng, Yong‐Tang; Tam, Siu-Cheung

doi:10.1016/j.lfs.2012.03.011

Cited by 7 publications

(8 citation statements)

References 34 publications

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“…3D). The findings of the present study and those of a previous study supported the hypothesis that treatment of uninfected HEp-2 cells with TCS prolongs the S-phase (6). The present study hypothesized that TCS may impair DNA replication through the induction of DNA damage.…”

Section: A B D Csupporting

confidence: 89%

“…Cancer cell line studies have indicated that TCS interferes with cell growth and causes apoptosis in cervical carcinoma HeLa cells, leukemia K562 and HL60 cells, gastric carcinoma MKN-45 cells and nasopharyngeal cancer CNE-1 cells (2,4). Several studies have also demonstrated that TCS treatment induces apoptosis and inhibits metastasis in human epithelial type 2 (HEp-2) human laryngeal epidermoid carcinoma cells (5,6). However, the mechanism by which TCS exerts its antitumor effects remains to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Low concentrations of trichosanthin induce apoptosis and cell cycle arrest via c-Jun N-terminal protein kinase/mitogen-activated protein kinase activation

Zhang

Chen

Zhou

et al. 2014

Molecular Medicine Reports

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Trichosanthin (TCS) is a type I ribosome--inactivating protein, which inhibits cell viability in human epithelial type 2 (HEp-2) and AMC-HN-8 human laryngeal epidermoid carcinoma cells. Although TCS is a potential chemotherapeutic agent, its mechanism of action remains to be elucidated. In the present study, HEp-2 and AMC-HN-8 cells were treated with different concentrations of TCS combined with or without cisplatin. After 5 days of successive treatment, different experimental groups were detected using a cell counting kit-8 and the collected supernatants were analyzed using a lactate dehydrogenase kit. Flow cytometric assays were performed to detect apoptosis and cell cycle arrest in the HEp-2 and AMC-HN-8 cells, reverse transcription quantitative polymerase chain reaction was performed to detect the levels of p27, p21WAF and western blot analysis was performed to detect changes in c-Jun N-terminal protein kinase (JNK)/phosphorylated (phospho)-JNK, p38/phospho-p38, extracellular signal-regulated kinase (ERK)/phospho-ERK, caspase-3 and caspase-9 in the HEp-2 and AMC-HN-8 cancer cells. TCS significantly inhibited the cell viability of the HEp-2 and AMC-HN-8 cells, independently of necrosis. TCS induced apoptosis and increased the percentage of HEp-2 and AMC-HN-8 cells in the S-phase of the cell cycle. In addition, the JNK/mitogen-activated protein kinase (MAPK) pathway was activated by TCS in the HEp-2 and AMC-HN-8 cells. Low concentrations of TCS also induced apoptosis and S-phase cell cycle arrest in the HEp-2 and AMC-HN-8 cells. The antitumor effects of TCS may be associated with JNK/MAPK activation.

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Section: A B D Csupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Low concentrations of trichosanthin induce apoptosis and cell cycle arrest via c-Jun N-terminal protein kinase/mitogen-activated protein kinase activation

Zhang

Chen

Zhou

et al. 2014

Molecular Medicine Reports

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“…It has been further shown that TCS could suppress the HSV-1 viral replication both in Vero cells and human epithelial carcinoma Hep-2 cells [ 74 , 75 ]. TCS may exert its anti-HSV virus activity via modulating three important signal pathways, namely p38 MAPK/Bcl2, nuclear factor-kappaB and p53 pathways ( Figure 3 ) [ 74 , 76 ]. TCS can suppress the elevation of p38 MAPK and Bcl-2 induced by HSV-1 infection to reduce viral replication in Vero cells [ 74 ].…”

Section: Tcs Possesses Multiple Pharmacological Propertiesmentioning

confidence: 99%

Structural and Functional Investigation and Pharmacological Mechanism of Trichosanthin, a Type 1 Ribosome-Inactivating Protein

Shi

Wong

Shaw

2018

Toxins

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Trichosanthin (TCS) is an RNA N-glycosidase that depurinates adenine-4324 in the conserved α-sarcin/ricin loop (α-SRL) of rat 28 S ribosomal RNA (rRNA). TCS has only one chain, and is classified as type 1 ribosome-inactivating protein (RIP). Our structural studies revealed that TCS consists of two domains, with five conserved catalytic residues Tyr70, Tyr111, Glu160, Arg163 and Phe192 at the active cleft formed between them. We also found that the structural requirements of TCS to interact with the ribosomal stalk protein P2 C-terminal tail. The structural analyses suggest TCS attacks ribosomes by first binding to the C-terminal domain of ribosomal P protein. TCS exhibits a broad spectrum of biological and pharmacological activities including anti-tumor, anti-virus, and immune regulatory activities. This review summarizes an updated knowledge in the structural and functional studies and the mechanism of its multiple pharmacological effects.

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“…TCS suppressed nasopharyngeal carcinomas via inhibiting Notch signaling and proliferation in vitro [115], as well as induced cell death and inhibited telomerase activity in nude mice [116]. Moreover, TCS possessed anti-HSV-1 property in human epithelial carcinoma cell line HEp-2 via type II apoptotic signaling after infection [117], and inhibiting the activation of NF-κB and inducing p53-dependent apoptosis [118]. TCS was used to successfully cure 85% of 140 cases of ectopic pregnancy with higher beta-human chorionic gonadotropin [119].…”

Section: Introductionmentioning

confidence: 99%

Bioactive proteins and peptides isolated from Chinese medicines with pharmaceutical potential

Wong

Zhang

et al. 2014

Chin Med

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Some protein pharmaceuticals from Chinese medicine have been developed to treat cardiovascular diseases, genetic diseases, and cancer. Bioactive proteins with various pharmacological properties have been successfully isolated from animals such as Hirudo medicinalis (medicinal leech), Eisenia fetida (earthworm), and Mesobuthus martensii (Chinese scorpion), and from herbal medicines derived from species such as Cordyceps militaris, Ganoderma, Momordica cochinchinensis, Viscum album, Poria cocos, Senna obtusifolia, Panax notoginseng, Smilax glabra, Ginkgo biloba, Dioscorea batatas, and Trichosanthes kirilowii. This article reviews the isolation methods, molecular characteristics, bioactivities, pharmacological properties, and potential uses of bioactive proteins originating from these Chinese medicines.

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The anti-herpetic activity of trichosanthin via the nuclear factor-κB and p53 pathways

Cited by 7 publications

References 34 publications

Low concentrations of trichosanthin induce apoptosis and cell cycle arrest via c-Jun N-terminal protein kinase/mitogen-activated protein kinase activation

Low concentrations of trichosanthin induce apoptosis and cell cycle arrest via c-Jun N-terminal protein kinase/mitogen-activated protein kinase activation

Structural and Functional Investigation and Pharmacological Mechanism of Trichosanthin, a Type 1 Ribosome-Inactivating Protein

Bioactive proteins and peptides isolated from Chinese medicines with pharmaceutical potential

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