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circ_0005962 functions as an oncogene to aggravate NSCLC progression

BACKGROUND: Non-small cell lung cancer (NSCLC) is a leading threat to human lives with high incidence and mortality. Circular RNAs were reported to play important roles in human cancers. The purpose of this study was to investigate the role of circ_0005962 and explore the underlying functional mecha...

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Autores principales: Zhang, Zhihong, Shan, Zhenxiu, Chen, Rubin, Peng, Xiaorong, Xu, Bin, Xiao, Liang, Zhang, Guofei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: De Gruyter 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8254573/
https://www.ncbi.nlm.nih.gov/pubmed/34250255
http://dx.doi.org/10.1515/med-2021-0255
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author Zhang, Zhihong
Shan, Zhenxiu
Chen, Rubin
Peng, Xiaorong
Xu, Bin
Xiao, Liang
Zhang, Guofei
author_facet Zhang, Zhihong
Shan, Zhenxiu
Chen, Rubin
Peng, Xiaorong
Xu, Bin
Xiao, Liang
Zhang, Guofei
author_sort Zhang, Zhihong
collection PubMed
description BACKGROUND: Non-small cell lung cancer (NSCLC) is a leading threat to human lives with high incidence and mortality. Circular RNAs were reported to play important roles in human cancers. The purpose of this study was to investigate the role of circ_0005962 and explore the underlying functional mechanisms. METHODS: The protein levels of Beclin 1, light chain3 (LC3-II/LC3-I), Pyruvate dehydrogenase kinase 4 (PDK4), Cleaved Caspase 3 (C-caspase 3), and proliferating cell nuclear antigen were examined using western blot analysis. Glycolysis was determined according to the levels of glucose consumption and lactate production. Xenograft model was constructed to investigate the role of circ_0005962 in vivo. RESULT: circ_0005962 expressed with a high level in NSCLC tissues and cells. circ_0005962 knockdown inhibited proliferation, autophagy, and glycolysis but promoted apoptosis in NSCLC cells. miR-382-5p was targeted by circ_0005962, and its inhibition reversed the role of circ_0005962 knockdown. Besides, PDK4, a target of miR-382-5p, was regulated by circ_0005962 through miR-382-5p, and its overexpression abolished the effects of miR-382-5p reintroduction. circ_0005962 knockdown suppressed tumor growth in vivo. CONCLUSION: circ_0005962 knockdown restrained cell proliferation, autophagy, and glycolysis but stimulated apoptosis through modulating the circ_0005962/miR-382-5p/PDK4 axis. Our study broadened the insights into understanding the mechanism of NSCLC progression.
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spelling pubmed-82545732021-07-08 circ_0005962 functions as an oncogene to aggravate NSCLC progression Zhang, Zhihong Shan, Zhenxiu Chen, Rubin Peng, Xiaorong Xu, Bin Xiao, Liang Zhang, Guofei Open Med (Wars) Research Article BACKGROUND: Non-small cell lung cancer (NSCLC) is a leading threat to human lives with high incidence and mortality. Circular RNAs were reported to play important roles in human cancers. The purpose of this study was to investigate the role of circ_0005962 and explore the underlying functional mechanisms. METHODS: The protein levels of Beclin 1, light chain3 (LC3-II/LC3-I), Pyruvate dehydrogenase kinase 4 (PDK4), Cleaved Caspase 3 (C-caspase 3), and proliferating cell nuclear antigen were examined using western blot analysis. Glycolysis was determined according to the levels of glucose consumption and lactate production. Xenograft model was constructed to investigate the role of circ_0005962 in vivo. RESULT: circ_0005962 expressed with a high level in NSCLC tissues and cells. circ_0005962 knockdown inhibited proliferation, autophagy, and glycolysis but promoted apoptosis in NSCLC cells. miR-382-5p was targeted by circ_0005962, and its inhibition reversed the role of circ_0005962 knockdown. Besides, PDK4, a target of miR-382-5p, was regulated by circ_0005962 through miR-382-5p, and its overexpression abolished the effects of miR-382-5p reintroduction. circ_0005962 knockdown suppressed tumor growth in vivo. CONCLUSION: circ_0005962 knockdown restrained cell proliferation, autophagy, and glycolysis but stimulated apoptosis through modulating the circ_0005962/miR-382-5p/PDK4 axis. Our study broadened the insights into understanding the mechanism of NSCLC progression. De Gruyter 2021-07-02 /pmc/articles/PMC8254573/ /pubmed/34250255 http://dx.doi.org/10.1515/med-2021-0255 Text en © 2021 Zhihong Zhang et al., published by De Gruyter https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License.
spellingShingle Research Article
Zhang, Zhihong
Shan, Zhenxiu
Chen, Rubin
Peng, Xiaorong
Xu, Bin
Xiao, Liang
Zhang, Guofei
circ_0005962 functions as an oncogene to aggravate NSCLC progression
title circ_0005962 functions as an oncogene to aggravate NSCLC progression
title_full circ_0005962 functions as an oncogene to aggravate NSCLC progression
title_fullStr circ_0005962 functions as an oncogene to aggravate NSCLC progression
title_full_unstemmed circ_0005962 functions as an oncogene to aggravate NSCLC progression
title_short circ_0005962 functions as an oncogene to aggravate NSCLC progression
title_sort circ_0005962 functions as an oncogene to aggravate nsclc progression
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8254573/
https://www.ncbi.nlm.nih.gov/pubmed/34250255
http://dx.doi.org/10.1515/med-2021-0255
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