دورية أكاديمية
Exosomal EGFR and miR-381-3P Mediate HPV-16 E7 Oncoprotein-Induced Angiogenesis of Non-Small Cell Lung Cancer.
| العنوان: | Exosomal EGFR and miR-381-3P Mediate HPV-16 E7 Oncoprotein-Induced Angiogenesis of Non-Small Cell Lung Cancer. |
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| المؤلفون: | Zhan R; Institute of Biochemistry and Molecular Biology, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China.; Collaborative Innovation Center for Antitumor Active Substance Research and Development, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China.; Department of Blood Transfusion, Affiliated Hospital of Guangdong Medical University, 524001 Zhanjiang, Guangdong, China., Yu H; Institute of Biochemistry and Molecular Biology, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China.; Collaborative Innovation Center for Antitumor Active Substance Research and Development, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China., Zhang G; Institute of Biochemistry and Molecular Biology, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China.; Collaborative Innovation Center for Antitumor Active Substance Research and Development, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China., Ding Q; Institute of Biochemistry and Molecular Biology, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China.; Collaborative Innovation Center for Antitumor Active Substance Research and Development, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China., Li H; Institute of Biochemistry and Molecular Biology, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China.; Collaborative Innovation Center for Antitumor Active Substance Research and Development, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China., Li X; Institute of Biochemistry and Molecular Biology, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China.; Collaborative Innovation Center for Antitumor Active Substance Research and Development, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China.; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Guangdong Medical University, 523808 Dongguan, Guangdong, China.; Dongguan Key Laboratory of Medical Bioactive Molecular Developmental and Translational Research, Guangdong Medical University, 523808 Dongguan, Guangdong, China., Tang X; Institute of Biochemistry and Molecular Biology, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China.; Collaborative Innovation Center for Antitumor Active Substance Research and Development, School of Basic Medicine, Guangdong Medical University, 524023 Zhanjiang, Guangdong, China.; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Guangdong Medical University, 523808 Dongguan, Guangdong, China.; Dongguan Key Laboratory of Medical Bioactive Molecular Developmental and Translational Research, Guangdong Medical University, 523808 Dongguan, Guangdong, China. |
| المصدر: | Frontiers in bioscience (Landmark edition) [Front Biosci (Landmark Ed)] 2024 May 15; Vol. 29 (5), pp. 189. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: IMR Press Country of Publication: Singapore NLM ID: 101612996 Publication Model: Print Cited Medium: Internet ISSN: 2768-6698 (Electronic) Linking ISSN: 27686698 NLM ISO Abbreviation: Front Biosci (Landmark Ed) Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2022- : Singapore : IMR Press Original Publication: Searington, NY : Frontiers in Bioscience |
| مواضيع طبية MeSH: | MicroRNAs*/genetics , MicroRNAs*/metabolism , Carcinoma, Non-Small-Cell Lung*/genetics , Carcinoma, Non-Small-Cell Lung*/metabolism , Carcinoma, Non-Small-Cell Lung*/pathology , Exosomes*/metabolism , Exosomes*/genetics , ErbB Receptors*/metabolism , ErbB Receptors*/genetics , Lung Neoplasms*/genetics , Lung Neoplasms*/metabolism , Lung Neoplasms*/pathology , Lung Neoplasms*/blood supply , Papillomavirus E7 Proteins*/genetics , Papillomavirus E7 Proteins*/metabolism , Neovascularization, Pathologic*/genetics , Neovascularization, Pathologic*/metabolism , Human Umbilical Vein Endothelial Cells*/metabolism , Cell Proliferation* , Cell Movement*, Humans ; Animals ; Cell Line, Tumor ; Mice ; Mice, Nude ; Human papillomavirus 16/genetics ; Angiogenesis |
| مستخلص: | Background: It has been demonstrated that exosomes derived from HPV-16 E7-over-expressiong non-small cell lung cancer (NSCLC) cells (E7 Exo) trigger increased levels of epidermal growth factor receptor (EGFR) and miR-381-3p. The purpose of this investigation was to examine the role of E7 Exo in NSCLC angiogenesis, and to analyze the contribution of exosomal EGFR and miR-381-3p to it. Methods: The influence of E7 Exo on the proliferation and migration of human umbilical vein endothelial cells (HUVECs) was assessed using colony formation and transwell migration assays. Experiments on both cells and animal models were conducted to evaluate the angiogenic effect of E7 Exo treatment. The involvement of exosomal EGFR and miR-381-3p in NSCLC angiogenesis was further investigated through suppressing exosome release or EGFR activation, or by over-expressing miR-381-3p. Results: Treatment with E7 Exo increased the proliferation, migration, and tube formation capacities of HUVECs, as well as angiogenesis in animal models. The suppression of exosome release or EGFR activation in NSCLC cells decreased the E7-induced enhancements in HUVEC migration and tube formation, and notably reduced vascular endothelial growth factor A (VEGFA) and Ang-1 levels. HUVECs that combined miR-381-3p mimic transfection and E7 Exo treatment exhibited a more significant tube-forming capacity than E7 Exo-treated HUVECs alone, but were reversed by the miR-381-3p inhibitor. Conclusion: The angiogenesis induced by HPV-16 E7 in NSCLC is mediated through exosomal EGFR and miR-381-3p. Competing Interests: The authors declare no conflict of interest. (© 2024 The Author(s). Published by IMR Press.) |
| معلومات مُعتمدة: | 2022KTSCX048 Characteristic Innovation Project of Guangdong Province Ordinary University (Nature Science) |
| فهرسة مساهمة: | Keywords: EGFR; HPV-16 E7; NSCLC; angiogenesis; exosomes; miR-381-3p |
| المشرفين على المادة: | 0 (MicroRNAs) EC 2.7.10.1 (ErbB Receptors) 0 (Papillomavirus E7 Proteins) 0 (oncogene protein E7, Human papillomavirus type 16) EC 2.7.10.1 (EGFR protein, human) 0 (MIRN381 microRNA, human) |
| تواريخ الأحداث: | Date Created: 20240530 Date Completed: 20240530 Latest Revision: 20240530 |
| رمز التحديث: | 20240530 |
| DOI: | 10.31083/j.fbl2905189 |
| PMID: | 38812317 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 2768-6698 |
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| DOI: | 10.31083/j.fbl2905189 |