Teroxirone suppresses growth and motility of human hepatocellular carcinoma cells

Kim, Seung Hun; Wang, Wen Hsing; Wang, Jing Ping; Hsieh, Chang Heng; Fang, Kang

doi:10.1016/j.biopha.2018.01.157

Cited by 5 publications

(2 citation statements)

References 30 publications

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“…Animal experiments have significant implications on the field of biomedicine [60, 61]. In this study, we tested the influence of lncRNA MALAT1 on atherosclerosis in vivo .…”

Section: Discussionmentioning

confidence: 99%

MALAT1/miR-15b-5p/MAPK1 mediates endothelial progenitor cells autophagy and affects coronary atherosclerotic heart disease via mTOR signaling pathway

Zhu

Yang

Duan

et al. 2019

Aging

111

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Objective: Present study focused on the influence of lncRNA MALAT1 on coronary atherosclerotic heart disease (CAD) by regulating miR-15b-5p/ MAPK1 and mTOR signaling pathway. Method: Differentially expressed genes and activated pathway were investigated through bioinformatics analysis. QRT-PCR was conducted to verify expression of MALAT1 , miR-15b-5p and MAPK1 in CAD blood samples and endothelial progenitor cells (EPCs). In addition, the interactions among MALAT1 , miR-15b-5p and MAPK1 were revealed by Luciferase reporter assay. Cell autophagy of EPCs was examined by Cyto-ID Autophagy Detection Kit and transmission electron microscope. MTT assay and flow cytometry were carried out to assess cell viability and apoptosis in different interference conditions. Western blot was performed to testify the expression of pERK1/2 (MAPK1), phosphorylated mTOR, ATG1 and LC3-II. Vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were detected by qRT-PCR. Finally, the effect of lncRNA MALAT1 on cell autophagy and atherogenesis was tested in vivo . Results: MALAT1 was overexpressed in CAD blood samples and EPCs. Knockdown of MALAT1 and MAPK1 promoted cell viability, autophagy and further suppressed the development of CAD. Antago MALAT1 protects mice against atherosclerosis. Conclusion: LncRNA MALAT1 inhibited EPCs autophagy and increased cell viability while repressed apoptosis of CAD via activating mTOR signaling pathway.

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“…Animal experiments have significant implications on the field of biomedicine [60, 61]. In this study, we tested the influence of lncRNA MALAT1 on atherosclerosis in vivo .…”

Section: Discussionmentioning

confidence: 99%

MALAT1/miR-15b-5p/MAPK1 mediates endothelial progenitor cells autophagy and affects coronary atherosclerotic heart disease via mTOR signaling pathway

Zhu

Yang

Duan

et al. 2019

Aging

111

View full text Add to dashboard Cite

show abstract

“…At present, many anti-cancer drug derivatives have been applied in the construction of drug-eluting stents, which can inhibit vascular remodeling by inhibiting the proliferation of VSMCs [24]. The heterocyclic trioxirane compound [1,3,5-tris((oxiran−2-yl)methyl)−1,3,5-triazinane−2,4,6trione (TGIC)] is a synthetic compound which has been used as an experimental anticancer agent in human clinical trial [25]. Preliminary structure-activity studies have shown that 1,3-disubstituted epoxypropyl groups are necessary for the maintenance of cytotoxicity.…”

Section: Introductionmentioning

confidence: 99%

OPN-modified nanoparticles loading BY1 inhibits vascular restenosis by inducing FTH1-dependent ferroptosis in vascular smooth muscle cells

Zhang,

Zheng,

Zhang

et al. 2023

Preprint

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Percutaneous coronary intervention has greatly improved the quality of life in patients with coronary artery disease. However, the vascular restenosis after angioplasty remains a challenging problem. Thus, there is still an urgent need to rationally design more effective drug and drug delivery system. In this study, the heterocyclic trioxirane compound [1, 3, 5-tris((oxiran-2-yl)methyl)-1, 3, 5-triazinane-2, 4, 6-trione (TGIC)], which has an anticancer activity, was used as the parent ring to conjugate with non-steroidal anti-inflammatory drug to obtain the spliced conjugated compound BY1, which is expected to prevent vascular remodeling. We found that BY1 potently induced ferroptosis in the cultured VSMCs as well as in neointima hyperplasia, accompanied by the significant accumulation of reactive oxygen species (ROS) and intracellular iron. The ferroptosis inducer and inhibitor enhanced and rescued, respectively, BY1-induced cell death, indicating that ferroptosis contributes to BY1-induced cell death in VSMCs. Further, we demonstrated that ferritin heavy chain1 (FTH1) was a key determinant for BY1-induced VSMC ferroptosis, as evidenced by the observations that FTH1 overexpression abrogated, while knockdown of FTH1 exacerbated, BY1-induced VSMC ferroptosis. Meanwhile, we compared the efficacy of different administration routes of BY1, including BY1-coated balloons, hydrogel-based BY1 delivery, and Osteopontin (OPN)-modified nanoparticles loading BY1 for targeting proliferated VSMCs (BY1-NP-OPN), for prevention and treatment of the restenosis. Our results suggest that BY1-NP-OPN is the most effective among the three administration routes, supporting the notion that BY1 might serve as a promising candidate for the development of drug coated stents or anti-restenosis drug.

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Nanoparticles targeting OPN loaded with BY1 inhibits vascular restenosis by inducing FTH1-dependent ferroptosis in vascular smooth muscle cells

Zhang,

Zheng,

Zhang

et al. 2024

Biomaterials

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Teroxirone suppresses growth and motility of human hepatocellular carcinoma cells

Cited by 5 publications

References 30 publications

MALAT1/miR-15b-5p/MAPK1 mediates endothelial progenitor cells autophagy and affects coronary atherosclerotic heart disease via mTOR signaling pathway

MALAT1/miR-15b-5p/MAPK1 mediates endothelial progenitor cells autophagy and affects coronary atherosclerotic heart disease via mTOR signaling pathway

OPN-modified nanoparticles loading BY1 inhibits vascular restenosis by inducing FTH1-dependent ferroptosis in vascular smooth muscle cells

Nanoparticles targeting OPN loaded with BY1 inhibits vascular restenosis by inducing FTH1-dependent ferroptosis in vascular smooth muscle cells

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