دورية أكاديمية
Antitumour effects of artesunate via cell cycle checkpoint controls in human oesophageal squamous carcinoma cells.
| العنوان: | Antitumour effects of artesunate via cell cycle checkpoint controls in human oesophageal squamous carcinoma cells. |
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| المؤلفون: | Mao L; Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.; State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.; Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, 310006, China., Deng G; Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.; State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China., Li M; Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.; State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China., Lu SH; Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.; State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.; Beijing Key Laboratory for Carcinogenesis and Cancer Prevention, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China., Jiang W; Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China. wjiang6138@cicams.ac.cn.; State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China. wjiang6138@cicams.ac.cn.; Beijing Key Laboratory for Carcinogenesis and Cancer Prevention, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China. wjiang6138@cicams.ac.cn., Yu X; Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China. yuxiying@cicams.ac.cn.; State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China. yuxiying@cicams.ac.cn.; Beijing Key Laboratory for Carcinogenesis and Cancer Prevention, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China. yuxiying@cicams.ac.cn. |
| المصدر: | European journal of medical research [Eur J Med Res] 2024 May 22; Vol. 29 (1), pp. 293. Date of Electronic Publication: 2024 May 22. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: BioMed Central Country of Publication: England NLM ID: 9517857 Publication Model: Electronic Cited Medium: Internet ISSN: 2047-783X (Electronic) Linking ISSN: 09492321 NLM ISO Abbreviation: Eur J Med Res Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Jan. 2012- : London : BioMed Central Original Publication: Munich, Germany : I. Holzapfel, c1995- |
| مواضيع طبية MeSH: | Artesunate*/pharmacology , Artesunate*/therapeutic use , Esophageal Neoplasms*/drug therapy , Esophageal Neoplasms*/metabolism , Esophageal Neoplasms*/genetics , Esophageal Neoplasms*/pathology , Esophageal Squamous Cell Carcinoma*/drug therapy , Esophageal Squamous Cell Carcinoma*/metabolism , Esophageal Squamous Cell Carcinoma*/pathology , Esophageal Squamous Cell Carcinoma*/genetics , Cell Cycle Checkpoints*/drug effects , Cell Proliferation*/drug effects , Apoptosis*/drug effects, Humans ; Animals ; Mice ; Cell Line, Tumor ; Mice, Nude ; Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology ; DNA Damage/drug effects ; Xenograft Model Antitumor Assays ; Artemisinins/pharmacology ; Artemisinins/therapeutic use ; Reactive Oxygen Species/metabolism ; Antineoplastic Agents/pharmacology |
| مستخلص: | Artesunate (ART), an effective antimalarial semisynthetic derivative of artemisinin, exhibits antitumour properties, but the mechanism(s) involved remain elusive. In this study, we investigated the antitumour effects of ART on human oesophageal squamous cell carcinoma (ESCC) cell lines. Treatment of ESCC cell lines with ART resulted in the production of excessive reactive oxygen species (ROS) that induced DNA damage, reduced cell proliferation and inhibited clonogenicity via G1-S cell cycle arrest and/or apoptosis in vitro. The administration of ART to nude mice with ESCC cell xenografts inhibited tumour formation in vivo. However, the cytotoxicity of ART strongly differed among the ESCC cell lines tested. Transcriptomic profiling revealed that although the expression of large numbers of genes in ESCC cell lines was affected by ART treatment, these genes could be functionally clustered into pathways involved in regulating cell cycle progression, DNA metabolism and apoptosis. We revealed that p53 and Cdk4/6-p16-Rb cell cycle checkpoint controls were critical determinants required for mediating ART cytotoxicity in ESCC cell lines. Specifically, KYSE30 cells with p53 Mut /p16 Mut were the most sensitive to ART, KYSE150 and KYSE180 cells with p53 Mut /p16 Nor exhibited intermediate responses to ART, and Eca109 cells with p53 Nor /p16 Nor exhibited the most resistance to ATR. Consistently, perturbation of p53 expression using RNA interference (RNAi) and/or Cdk4/6 activity using the inhibitor palbociclib altered ART cytotoxicity in KYSE30 cells. Given that the p53 and Cdk4/6-cyclin D1-p16-Rb genes are commonly mutated in ESCC, our results potentially shed new light on neoadjuvant chemotherapy strategies for ESCC. (© 2024. The Author(s).) |
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| فهرسة مساهمة: | Keywords: Artesunate; DNA damage and cell cycle checkpoint controls; Oesophageal squamous cell carcinoma; Reactive oxygen species |
| تواريخ الأحداث: | Date Created: 20240521 Date Completed: 20240522 Latest Revision: 20240524 |
| رمز التحديث: | 20240524 |
| مُعرف محوري في PubMed: | PMC11110347 |
| DOI: | 10.1186/s40001-024-01882-9 |
| PMID: | 38773551 |
| قاعدة البيانات: | MEDLINE |
Find this article in full text from Springer Verlag. 
Full Text Finder | تدمد: | 2047-783X |
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| DOI: | 10.1186/s40001-024-01882-9 |