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Serum-Derived Exosomes-Mediated Circular RNA ARHGAP10 Modulates the Progression of Non-Small Cell Lung Cancer Through the miR-638/FAM83F Axis.
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- Author(s): Fang K;Fang K; Chen X; Chen X; Qiu F; Qiu F; Xu J; Xu J; Xiong H; Xiong H; Zhang Z; Zhang Z
- Source:
Cancer biotherapy & radiopharmaceuticals [Cancer Biother Radiopharm] 2022 Mar; Vol. 37 (2), pp. 96-110. Date of Electronic Publication: 2020 Aug 12.- Publication Type:
Journal Article- Language:
English - Source:
- Additional Information
- Source: Publisher: Mary Ann Liebert, Inc Country of Publication: United States NLM ID: 9605408 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1557-8852 (Electronic) Linking ISSN: 10849785 NLM ISO Abbreviation: Cancer Biother Radiopharm Subsets: MEDLINE
- Publication Information: Original Publication: Larchmont, NY : Mary Ann Liebert, Inc., c1996-
- Subject Terms:
- Abstract: Background: Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths all over the world. Exosomes exert central roles in intercellular communication. Circular RNA Rho GTPase activating protein 10 (circARHGAP10) was related to the development of NSCLC. Nevertheless, it was unclear whether circARHGAP10 can be mediated by serum-derived exosomes in NSCLC. Materials and Methods: Protein expression of CD63, CD81, family with sequence similarity 83F (FAM83F), glucose transporter 1 (Glut1), and lactate dehydrogenase were evaluated through Western blot analysis. The expression of circARHGAP10, miR-638, and FAM83F was examined by quantitative real-time polymerase chain reaction. Cell proliferation, migration, and invasion were evaluated through 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) or transwell assays. Glucose consumption and lactate production were analyzed with special commercial kits. The relationship between circARHGAP10 or FAM83F and miR-638 was identified by dual-luciferase reporter or RNA immunoprecipitation (RIP) assays. The role of circARHGAP10 in vivo was confirmed through xenograft assay. Results: circARHGAP10 was upregulated in NSCLC tissues, cells, and serum-derived exosomes. Serum-derived exosomes boosted the expression of circARHGAP10 in NSCLC cells. circARHGAP10 depletion repressed proliferation, migration, invasion, and glycolysis of NSCLC cells in vitro , and curbed tumor growth in vivo . Also, miR-638 acted as a target of circARHGAP10, miR-638 overexpression overturned circARHGAP10 upregulation-mediated acceleration of proliferation, migration, invasion, and glycolysis of NSCLC cells. Besides, miR-638 targeted FAM83F and FAM83F overexpression abolished miR-638 enhancement-mediated proliferation, migration, invasion, and glycolysis of NSCLC cells. Conclusions: Inhibition of serum-derived exosomes-mediated circARHGAP10 curbed NSCLC progression through the miR-638/FAM83F axis.
- Contributed Indexing: Keywords: FAM83F; NSCLC; circARHGAP10; exosomes; miR-638
- Accession Number: 0 (MIRN638 microRNA, human)
0 (MicroRNAs)
0 (RNA, Circular) - Publication Date: Date Created: 20200814 Date Completed: 20220318 Latest Revision: 20220531
- Publication Date: 20240105
- Accession Number: 10.1089/cbr.2019.3534
- Accession Number: 32783691
- Source:
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