Nianxi Tan, Junyi Tang, Guang Chen, Weilin Jiang, Zhiqin Liu
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Knockdown of ZEB1-AS1 resulted in a significant suppression of cell viability, proliferation, migration, invasion, and EMT in A549 cells. Furthermore, we confirmed the targeting relationship between ZEB1-AS1 and miR-320b, as well as between miR-320b and BMPR1A. Our findings suggested that ZEB1-AS1 regulated cell viability, proliferation, migration, and invasion, as well as EMT, in lung cancer cells by targeting the miR-320b/BMPR1A axis. Moreover, our in vivo experiments confirmed that ZEB1-AS1 mediated bone metastasis through targeting miR-320b/BMPR1A axis in mice with lung cancer.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>ZEB1-AS1 mediated bone metastasis through targeting miR-320b/BMPR1A axis in lung cancer.</p>\n </section>\n </div>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"18 5","pages":""},"PeriodicalIF":1.9000,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.13770","citationCount":"0","resultStr":"{\"title\":\"ZEB1-AS1 mediates bone metastasis through targeting miR-320b/BMPR1A axis in lung cancer\",\"authors\":\"Nianxi Tan, Junyi Tang, Guang Chen, Weilin Jiang, Zhiqin Liu\",\"doi\":\"10.1111/crj.13770\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Objective</h3>\\n \\n <p>This study aimed to explore the role and regulatory mechanism of lncRNA ZEB1-AS1 in lung cancer.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methods</h3>\\n \\n <p>The expression of ZEB1-AS1 and miR-320b was determined by qRT-PCR. Cell viability, proliferation migration, and invasion were assessed using the CCK-8, colony-forming, and Transwell assay. EMT markers were quantified using western blot. The growth of subcutaneous tumor growth and metastatic bone tumors was evaluated in mouse model of lung cancer. Additionally, metastatic bone tumors were examined using H&E staining.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>ZEB1-AS1 expression was upregulated, while miR-320b levels were downregulated in lung cancer. Knockdown of ZEB1-AS1 resulted in a significant suppression of cell viability, proliferation, migration, invasion, and EMT in A549 cells. Furthermore, we confirmed the targeting relationship between ZEB1-AS1 and miR-320b, as well as between miR-320b and BMPR1A. Our findings suggested that ZEB1-AS1 regulated cell viability, proliferation, migration, and invasion, as well as EMT, in lung cancer cells by targeting the miR-320b/BMPR1A axis. 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ZEB1-AS1 mediates bone metastasis through targeting miR-320b/BMPR1A axis in lung cancer
Objective
This study aimed to explore the role and regulatory mechanism of lncRNA ZEB1-AS1 in lung cancer.
Methods
The expression of ZEB1-AS1 and miR-320b was determined by qRT-PCR. Cell viability, proliferation migration, and invasion were assessed using the CCK-8, colony-forming, and Transwell assay. EMT markers were quantified using western blot. The growth of subcutaneous tumor growth and metastatic bone tumors was evaluated in mouse model of lung cancer. Additionally, metastatic bone tumors were examined using H&E staining.
Results
ZEB1-AS1 expression was upregulated, while miR-320b levels were downregulated in lung cancer. Knockdown of ZEB1-AS1 resulted in a significant suppression of cell viability, proliferation, migration, invasion, and EMT in A549 cells. Furthermore, we confirmed the targeting relationship between ZEB1-AS1 and miR-320b, as well as between miR-320b and BMPR1A. Our findings suggested that ZEB1-AS1 regulated cell viability, proliferation, migration, and invasion, as well as EMT, in lung cancer cells by targeting the miR-320b/BMPR1A axis. Moreover, our in vivo experiments confirmed that ZEB1-AS1 mediated bone metastasis through targeting miR-320b/BMPR1A axis in mice with lung cancer.
Conclusion
ZEB1-AS1 mediated bone metastasis through targeting miR-320b/BMPR1A axis in lung cancer.
期刊介绍：
Overview
Effective with the 2016 volume, this journal will be published in an online-only format.
Aims and Scope
The Clinical Respiratory Journal (CRJ) provides a forum for clinical research in all areas of respiratory medicine from clinical lung disease to basic research relevant to the clinic.
We publish original research, review articles, case studies, editorials and book reviews in all areas of clinical lung disease including:
Asthma
Allergy
COPD
Non-invasive ventilation
Sleep related breathing disorders
Interstitial lung diseases
Lung cancer
Clinical genetics
Rhinitis
Airway and lung infection
Epidemiology
Pediatrics
CRJ provides a fast-track service for selected Phase II and Phase III trial studies.
Keywords
Clinical Respiratory Journal, respiratory, pulmonary, medicine, clinical, lung disease,
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Journal Citation Reports/Science Edition (Clarivate Analytics)
MEDLINE/PubMed (NLM)
ProQuest Central (ProQuest)
Science Citation Index Expanded (Clarivate Analytics)
SCOPUS (Elsevier)
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