Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axis

Background Propofol has been reported to be related to the migration, invasion, and epithelial‐mesenchymal transition (EMT) of esophageal cancer (EC) cells. However, the detailed mechanism has not yet been fully reported. The purpose of this research was to elucidate the function of long non‐coding...

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Main Authors: Meng Gao, Rui Guo, Xihua Lu, Gang Xu, Suxia Luo
Format: Article
Language:English
Published: Wiley 2020-09-01
Series:Thoracic Cancer
Subjects:
Online Access:https://doi.org/10.1111/1759-7714.13534
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author Meng Gao
Rui Guo
Xihua Lu
Gang Xu
Suxia Luo
author_facet Meng Gao
Rui Guo
Xihua Lu
Gang Xu
Suxia Luo
author_sort Meng Gao
collection DOAJ
description Background Propofol has been reported to be related to the migration, invasion, and epithelial‐mesenchymal transition (EMT) of esophageal cancer (EC) cells. However, the detailed mechanism has not yet been fully reported. The purpose of this research was to elucidate the function of long non‐coding RNA TMPO antisense RNA 1 (lncRNA TMPO‐AS1) and microRNA‐498 (miR‐498) in propofol‐regulated EC. Methods Transwell assay was performed to assess cell migratory and invasive abilities. Western blot assay was employed to determine the levels of EMT markers and hypoxia inducible factor‐1 (HIF‐1α). Quantitative real‐time polymerase chain reaction (qRT‐PCR) was carried out to detect the levels of TMPO‐AS1 and miR‐498. Moreover, the interaction between TMPO‐AS1 and miR‐498 was predicted by starBase, and then confirmed by the dual‐luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results Propofol suppressed hypoxia‐induced EC cell migration, invasion, and EMT. Both TMPO‐AS1 overexpression and miR‐498 knockdown weakened the effect of propofol on hypoxia‐induced EC cell progression. Interestingly, TMPO‐AS1 targeted miR‐498 and suppressed miR‐498 expression. TMPO‐AS1 regulated EC cell progression via downregulating miR‐498 expression. Conclusions Collectively, our findings demonstrated that propofol inhibited hypoxia‐induced EC cell mobility through modulation of the TMPO‐AS1/miR‐498 axis, providing a theoretical basis for the treatment of EC.
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spelling doaj.art-f9d213611c7442e58d7b2f38c6c626022022-12-21T18:25:10ZengWileyThoracic Cancer1759-77061759-77142020-09-011192398240510.1111/1759-7714.13534Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axisMeng Gao0Rui Guo1Xihua Lu2Gang Xu3Suxia Luo4Department of Anesthesiology Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital Zhengzhou ChinaDepartment of Clinical Laboratory Henan Provincial People's Hospital, People's Hospital of Zhengzhou University Zhengzhou Zhengzhou ChinaDepartment of Anesthesiology Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital Zhengzhou ChinaDepartment of Anesthesiology Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital Zhengzhou ChinaDepartment of Medical Oncology Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital Zhengzhou ChinaBackground Propofol has been reported to be related to the migration, invasion, and epithelial‐mesenchymal transition (EMT) of esophageal cancer (EC) cells. However, the detailed mechanism has not yet been fully reported. The purpose of this research was to elucidate the function of long non‐coding RNA TMPO antisense RNA 1 (lncRNA TMPO‐AS1) and microRNA‐498 (miR‐498) in propofol‐regulated EC. Methods Transwell assay was performed to assess cell migratory and invasive abilities. Western blot assay was employed to determine the levels of EMT markers and hypoxia inducible factor‐1 (HIF‐1α). Quantitative real‐time polymerase chain reaction (qRT‐PCR) was carried out to detect the levels of TMPO‐AS1 and miR‐498. Moreover, the interaction between TMPO‐AS1 and miR‐498 was predicted by starBase, and then confirmed by the dual‐luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results Propofol suppressed hypoxia‐induced EC cell migration, invasion, and EMT. Both TMPO‐AS1 overexpression and miR‐498 knockdown weakened the effect of propofol on hypoxia‐induced EC cell progression. Interestingly, TMPO‐AS1 targeted miR‐498 and suppressed miR‐498 expression. TMPO‐AS1 regulated EC cell progression via downregulating miR‐498 expression. Conclusions Collectively, our findings demonstrated that propofol inhibited hypoxia‐induced EC cell mobility through modulation of the TMPO‐AS1/miR‐498 axis, providing a theoretical basis for the treatment of EC.https://doi.org/10.1111/1759-7714.13534Esophageal cancerhypoxiamiR‐498propofolTMPO‐AS1
spellingShingle Meng Gao
Rui Guo
Xihua Lu
Gang Xu
Suxia Luo
Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axis
Thoracic Cancer
Esophageal cancer
hypoxia
miR‐498
propofol
TMPO‐AS1
title Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axis
title_full Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axis
title_fullStr Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axis
title_full_unstemmed Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axis
title_short Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axis
title_sort propofol suppresses hypoxia induced esophageal cancer cell migration invasion and emt through regulating lncrna tmpo as1 mir 498 axis
topic Esophageal cancer
hypoxia
miR‐498
propofol
TMPO‐AS1
url https://doi.org/10.1111/1759-7714.13534
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