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2-Methoxy-5((3,4,5-trimethosyphenyl) seleninyl) phenol causes G2/M cell cycle arrest and apoptosis in NSCLC cells through mitochondrial apoptotic pathway and MDM2 inhibition.
Liu, Yang; Meng, Yuting; Bian, Jiang; Liu, Bolin; Li, Xuefen; Guan, Qi; Li, Zengqiang; Zhang, Weige; Wu, Yingliang; Zuo, Daiying.
Afiliación
  • Liu Y; Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, China.
  • Meng Y; Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, China.
  • Bian J; Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, China.
  • Liu B; College of Pharmacy, China Medical University, Shenyang, China.
  • Li X; Department of Pharmacy, Inner Mongolia Hospital of Traditional Chinese Medicine, Hohhot, China.
  • Guan Q; Key Laboratory of Structure-Based Drug Design and Discovery, Ministry of Education, Shenyang Pharmaceutical University, Shenyang, China.
  • Li Z; Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, China.
  • Zhang W; Key Laboratory of Structure-Based Drug Design and Discovery, Ministry of Education, Shenyang Pharmaceutical University, Shenyang, China.
  • Wu Y; Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, China.
  • Zuo D; Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, China.
J Biochem Mol Toxicol ; 36(7): e23066, 2022 Jul.
Article en En | MEDLINE | ID: mdl-35384151
Nonsmall cell lung cancer (NSCLC) is one of the most common malignancies and needs novel and effective chemotherapy. In this study, our purpose is to explore the anticancer effects of 2-methoxy-5((3,4,5-trimethosyphenyl) seleninyl) phenol (SQ) on human NSCLC (A549 and H460) cells. We found that SQ suppressed the proliferation of NSCLC cells in time- and dose-dependent manners, and blocked the cells at G2/M phase, which was relevant to microtubule depolymerization. Additionally, SQ induced A549 and H460 cell apoptosis by activating the mitochondrial apoptotic pathway. Further, we demonstrated that SQ enhanced the generation of reactive oxygen species (ROS), and pretreatment with N-acetyl- L-cysteine (NAC) attenuated SQ-induced cell apoptosis. Meanwhile, SQ mediated-ROS generation caused DNA damage in A549 and H460 cells. Our data also revealed that SQ-induced apoptosis was correlated with the inhibition of mouse double minute 2 (MDM2) in A549 and H460 cells. In summary, our research indicates that the novel compound SQ has great potential for therapeutic treatment of NSCLC in future.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Carcinoma de Pulmón de Células no Pequeñas / Proteínas Proto-Oncogénicas c-mdm2 / Neoplasias Pulmonares Tipo de estudio: Etiology_studies Límite: Animals / Humans Idioma: En Revista: J Biochem Mol Toxicol Asunto de la revista: BIOLOGIA MOLECULAR / BIOQUIMICA / TOXICOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Carcinoma de Pulmón de Células no Pequeñas / Proteínas Proto-Oncogénicas c-mdm2 / Neoplasias Pulmonares Tipo de estudio: Etiology_studies Límite: Animals / Humans Idioma: En Revista: J Biochem Mol Toxicol Asunto de la revista: BIOLOGIA MOLECULAR / BIOQUIMICA / TOXICOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos