Pseudolaric acid B inhibits proliferation in SW579 human thyroid squamous cell carcinoma

Iodine-131 (131I) is widely used for the treatment of thyroid-related diseases. This study aimed to investigate the expression of p53 and BTG2 genes following 131I therapy in thyroid cancer cell line SW579 and the possible underlying mechanism. SW579 human thyroid squamous carcinoma cells were cultured and treated with 131I. They were then assessed for 131I uptake, cell viability, apoptosis, cell cycle arrest, p53 expression, and BTG2 gene expression. SW579 cells were transfected with BTG2 siRNA, p53 siRNA and siNC and were then examined for the same aforementioned parameters. When treated with a JNK inhibitor of SP600125 and 131I or with a NF-κB inhibitor of BMS-345541 and 131I, non-transfected SW579 cells were assessed in JNK/NFκB pathways. It was observed that 131I significantly inhibited cell proliferation, promoted cell apoptosis and cell cycle arrest. Both BTG2 and p53 expression were enhanced in a dose-dependent manner. An increase in cell viability by up-regulation in Bcl2 gene, a decrease in apoptosis by enhanced CDK2 gene expression and a decrease in cell cycle arrest at G0/G1 phase were also observed in SW579 cell lines transfected with silenced BTG2 gene. When treated with SP600125 and 131I, the non-transfected SW579 cell lines significantly inhibited JNK pathway, NF-κB pathway and the expression of BTG2. However, when treated with BMS-345541 and 131I, only the NF-κB pathway was suppressed. 131I suppressed cell proliferation, induced cell apoptosis, and promoted cell cycle arrest of thyroid cancer cells by up-regulating B-cell translocation gene 2-mediated activation of JNK/NF-κB pathways.

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“…SP600125 (10 μM) and BMS-345541 (10 μM) were used as JNK and NF-κB inhibitors to treat SW579 for 3 days, respectively (16). …”

Section: Methodsmentioning

confidence: 99%

Iodine-131 treatment of thyroid cancer cells leads to suppression of cell proliferation followed by induction of cell apoptosis and cell cycle arrest by regulation of B-cell translocation gene 2-mediated JNK/NF-κB pathways

Zhao

Pang

2017

Braz J Med Biol Res

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“…PAB promotes the aggregation of microtubule fiber. PAB exerts its function by influencing microtubule fiber aggregation (17). We found that PAB treatment promoted the uneven aggregation of microtubule fibers with more obvious red staining, while control cells showed even aggregation of microtubule fibers (Fig.…”

Section: Resultsmentioning

confidence: 75%

Pseudolaric acid B inhibits neuroglioma cell proliferation through DNA damage response

Song

Zhang

et al. 2017

Oncology Reports

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Human neuroglioma is one of the most common malignant intracranial tumors in neurosurgery, and accounts for more than 50% of all brain cancer cases. Thus, a clinically effective drug with which to treat neuroglioma is urgently required. Pseudolaric acid B (PAB), a diterpene acid isolated from the root and trunk bark of Pseudolarix kaempferi Gordon (Pinaceae), was found to inhibit cell growth in a variety of cancer cell lines, but to date the effect of PAB on neuroglioma remains unclear. MTT analysis confirmed that PAB inhibited neuroglioma A172 cell growth in a time- and dose-dependent manner. In addition, PAB influenced the aggregation of tubulin in A172 cells. Meanwhile following PAB treatment, a higher percentage of cells accumulated in the G2/M phase from 12 to 48 h, while at 36 h, cell cycle slippage into the G0/G1 phase, and at 48 h, slippage into the S phase was observed using flow cytometric analysis. Corresponding protein expression was consistent with the cell cycle alteration as detected by western blotting, and it was speculated that cell cycle slippage was related to reduced effectiveness of PAB which warrants further investigation. Meanwhile PAB induced cell death by regulating p38, ERK and JNK expression and activating the DNA damage response. Therefore, PAB plays an antitumor role in A172 cells, and may be a candidate drug for neuroglioma therapy.

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“…It is worth noting that pseudolaric acid B, oridonin, and erianin were extracted from P. kaempferi Grord ( Pinaceae ; Yu et al, ; Yu et al, ; Yu et al, ; Yu et al, ; Yu, Li, et al, ; Yu, Ren, et al, ; Yu, Wang, et al, ), R. rubescens (Li et al, ; Ye et al, ) and Dendrobium chrysotoxum (Wang et al, ), respectively, which should be considered for treating EVD68‐related diseases. However, rheum emodin, artemisinin, and astragaloside were extracted from Chinese rhubarb (also from Polygonum cuspidatum Sieb.et Zucc, Rumex patientia Linn, Fagopyrum dibotrys (D.Don) Hara, Rumex japonicus Houtt, Fallopia multiflora (Thunb.)…”

Section: Discussionmentioning

confidence: 99%

“…A major saponin of this herb, astragaloside, has anticancer, antifatigue, anti‐Coxsackie B virus, and anti‐inflammatory effects (Chen et al, ). Pseudolaric acid B, which is a diterpene acid isolated from the roots and trunk bark of Pseudolarix kaempferi Grord ( Pinaceae ), has antifungal (Li, Clark, & Hufford, ) and antitumor activities (Yu et al, ; Yu et al, ; Yu et al, ; Yu et al, ; Yu et al, ; Yu, Li, Tashiro, Onodera, & Ikejima, ; Yu, Wang, et al, ). Oridonin, an active diterpenoid isolated from Rabdosia rubescens , has antitumor (Li et al, ; Ye et al, ) and anti‐inflammatory (Zhao et al, ) effects.…”

Section: Introductionmentioning

confidence: 99%

Effect of ingredients from Chinese herbs on enterovirus D68 production

Meng

Liu

et al. 2018

Phytotherapy Research

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Human enterovirus 68 (EVD68) is a primary causative agent for respiratory illness worldwide. Until now, there has been no available medication for treating EVD68related diseases. Rheum emodin, artemisinin, astragaloside, pseudolaric acid B, oridonin, and erianin are natural extracts from Chinese herbs that have traditionally been used for the treatment and prevention of epidemic diseases. Our results showed that pseudolaric acid B protected cells from EVD68-induced cytopathic effects and decreased viral production. However, the same effects were not observed with rheum emodin, astragaloside, or artemisinin. Pseudolaric acid B inhibited EVD68 production by manipulating the host cell cycle in G2/M phase. Further, either oridonin or erianin related G2/M arrest also inhibited viral production. Due to inducing G2/M phase arrest, pseudolaric acid B, oridonin, and erianin might be good candidates for inhibiting EVD68 production, and Chinese herbs with natural compounds inducing G2/M arrest should be considered for the treatment of EVD68-related diseases. KEYWORDS enterovirus D68 (EVD68), G2/M arrest, natural compounds, viral production

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Pseudolaric acid B inhibits proliferation in SW579 human thyroid squamous cell carcinoma

Cited by 20 publications

References 25 publications

Iodine-131 treatment of thyroid cancer cells leads to suppression of cell proliferation followed by induction of cell apoptosis and cell cycle arrest by regulation of B-cell translocation gene 2-mediated JNK/NF-κB pathways

Iodine-131 treatment of thyroid cancer cells leads to suppression of cell proliferation followed by induction of cell apoptosis and cell cycle arrest by regulation of B-cell translocation gene 2-mediated JNK/NF-κB pathways

Pseudolaric acid B inhibits neuroglioma cell proliferation through DNA damage response

Effect of ingredients from Chinese herbs on enterovirus D68 production

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