Pseudolaric acid B induces apoptosis in human rhabdomyosarcoma RD cells

Liu, Chunyu; Wang, Fei; Wang, Bin; Wu, Ting; Wang, Yue; Huo, Wenbo; Zhang, Shuxia; Su, Ying; Liu, Yumeng; Yu, Jinghua

doi:10.3892/ol.2020.12222

Cited by 3 publications

(2 citation statements)

References 22 publications

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“…Immunofluorescence staining of MRC-5 cells was performed as previously described ( 41 ). MRC-5 cells plated onto cover glasses were fixed with 4% paraformaldehyde for 15 min and then blocked in 5% BSA for 1 h both at room temperature.…”

Section: Methodsmentioning

confidence: 99%

lncRNA GAS5 promotes pyroptosis in COPD by functioning as a ceRNA to regulate the miR‑223‑3p/NLRP3 axis

Chen

et al. 2022

Mol Med Rep

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Chronic obstructive pulmonary disease (COPD) is characterized by irreversible and progressive airflow limitation and encompasses a spectrum of diseases, including chronic obstructive bronchitis and emphysema. Pyroptosis is a unique form of inflammatory cell death mediated by the activation of caspase-1 and inflammasomes. The long non-coding RNA (lncRNA) growth arrest-specific 5 (GAS5) is a well-documented tumor suppressor, which is associated with cell proliferation and death in various diseases. The aim of the present study was to evaluate whether lncRNA GAS5 is associated with the pyroptosis in COPD. To create a COPD cell model, MRC-5 cells were treated with 10 µg/ml lipopolysaccharide (LPS) for 48 h. Then the level of pro-caspase 1, caspase 1, IL-1β, IL-18, NLRP3 and cleaved gasdermin D (GSDMD) was examined by western blotting. GAS5 mRNA level was detected by qualitative PCR following LPS treatment in MRC-5 cells. Subsequently, IL-2, IL-6, IL-10 and TNF-α in MRC-5 cells was measured by ELISA. Then the proliferation ability of MRC-5 cells was detected by CCK-8. Cell death was detected by TUNEL assay. LDH release was measured using an LDH Cytotoxicity Assay kit. The Magna RIP kit was used to validate the interaction between GAS5 and miR-223-3p. The present study revealed that increased expression levels of caspase-1, IL-1β, IL-18 and cleaved GSDMD were observed in LPS-treated MRC-5 cells, indicating that pyroptosis is involved in COPD progression. Additionally, LPS induced the increase in GAS5 mRNA expression levels and the release of inflammatory factors (IL-2, IL-6, IL-10 and TNF-α), suggesting that GAS5 is implicated in pyroptosis in COPD. Furthermore, upregulation of GAS5 promoted cell death and inhibited proliferation in the MRC-5 cell line. Additionally, increased GAS5 expression significantly promoted the production of caspase-1, IL-1β, IL-18, cleaved GSDMD and NLR pyrin domain containing protein 3 (NLRP3). A dual-luciferase assay demonstrated that GAS5 could directly bind to microRNA-223-3p (miR-223-3p), and NLRP3 is a direct target of miR-223-3p. Furthermore, GAS5 reduced the expression levels of miR-223-3p, while it increased the expression levels of NLRP3. The present study concluded that lncRNA GAS5 promoted pyroptosis in COPD by targeting the miR-223-3p/NLRP3 axis, implying that GAS5 could be a potential target for COPD.

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Section: Methodsmentioning

confidence: 99%

lncRNA GAS5 promotes pyroptosis in COPD by functioning as a ceRNA to regulate the miR‑223‑3p/NLRP3 axis

Chen

et al. 2022

Mol Med Rep

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“…In short, PAB exhibits a strong parasiticidal effect on E. multilocularis larvae both in vitro and in vivo. Previous study demonstrated that PAB exerts antitumor effects by activated apoptosis, autophagy and cell cycle arrest in certain types of cancer cells (Yu et al, 2008, Liu et al, 2020a. It was recognized that TGF-β1 signaling could trigger a variety of cellular responses, including inhibition of cell growth, migration, differentiation and apoptosis (Sanchez-Capelo, 2005).…”

Section: Groupmentioning

confidence: 99%

Suppressive effect of pseudolaric acid B on Echinococcus multilocularis involving regulation of TGF-β1 signaling in vitro and in vivo

Gao

Huo

et al. 2022

Front. Microbiol.

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Echinococcus multilocularis, the causative agent of alveolar echinococcosis (AE), severely threats human health and livestock farming. The first line of chemotherapeutic drug for AE is albendazole, which limits rapid extension of E. multilocularis metacestodes, but is rarely curative for AE, with severe side effects in long-term use, thus development of new anti-echinococcal drugs is mandated. Pseudolaric acid B (PAB) has long been used to treat fungal-infected dermatosis, and exerted anti-tumor, -fertility, -angiogenesis, -tubulin and antiparasitic activity. However, the effect of PAB against Echinococcus spp. remains unclear. The present study is to understand the effect of PAB against E. multilocularis in vitro and in vivo, and identify potential anti-echinococcal mechanism, as well as its toxicity. After exposure to PAB at 20 μg/ml, significant reduction of the survival rate and substantial ultrastructural destructions in E. multilocularis protoscoleces were observed in vitro. Furthermore, the wet weight of E. multilocularis cysts in the infected mice was significantly decreased after treatment with PAB (40, 20 or 10 mg/kg) for 12 weeks. Meanwhile, significant increase of both protein and mRNA expression of transforming growth factor beta 1 (TGF-β1) was detected in the serum and liver of the infected mice, whereas PAB administration lowered its expression significantly. The toxicity tests demonstrated that PAB displayed lower cytotoxicity to human liver and kidney cells (HL-7702 and HK-2 cell) with IC50 = 25.29 and 42.94 μg/ml than albendazole with IC50 = 3.71 and 21.22 μg/ml in vitro, and caused lower hepatoxicity and nephrotoxicity in mice than ABZ. Our findings indicated that PAB possesses potent anti-echinococcal effect, with lower toxicity than albendazole, implying a potential chemotherapeutic agent for AE. Additionally, the present study demonstrated that the suppressive effect of PAB on the parasite may involve down-regulation of TGF-β1 signaling.

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Ferroptosis molecular inducers: A future direction for malignant tumor chemotherapy

Wang¹,

LI²,

WANG³

et al. 2022

Biocell

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Iron-dependent ferroptosis is a form of cell death dependent on iron levels. Cells that undergo ferroptosis have glutathione (GSH) deficiency, reduced Glutathione peroxidase-4 (GPX4) activity and intracellular lipid peroxidation, Mitochondria, lysosomes and many signal pathways are involved in the regulation of ferroptosis. More importantly, many tumor cells resistant to other cell death methods exhibit sensitivity to ferroptosis. Moreover, over recent years, a number of ferroptosis-induced drugs have been recommended for the treatment of malignant tumors. Therefore, the study of ferroptosis is of great significance for future cancer treatments. In this review, we discussed the metabolic process of ferroptosis, the role of different organelles, the typical signaling pathways involved in ferroptosis, as well as natural and synthetic compounds that can induce ferroptosis, aiming to point out new conceptual avenues for utilizing ferroptosis in future cancer treatments.

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Pseudolaric acid B induces apoptosis in human rhabdomyosarcoma RD cells

Cited by 3 publications

References 22 publications

lncRNA GAS5 promotes pyroptosis in COPD by functioning as a ceRNA to regulate the miR‑223‑3p/NLRP3 axis

lncRNA GAS5 promotes pyroptosis in COPD by functioning as a ceRNA to regulate the miR‑223‑3p/NLRP3 axis

Suppressive effect of pseudolaric acid B on Echinococcus multilocularis involving regulation of TGF-β1 signaling in vitro and in vivo

Ferroptosis molecular inducers: A future direction for malignant tumor chemotherapy

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