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Linc01614 Regulates the Proliferation, Apoptosis, and Chemotherapy Resistance in Esophageal Squamous Cell Carcinoma by Targeting Mir-4775

BACKGROUND: Esophageal squamous cell carcinoma (ESCC), a widely known esophageal disease, severely affects people’s health. Numerous investigations demonstrated that long non-coding RNAs (lncRNAs) performed key jobs inside a wide scope of organic cycles and stand out in malignant growth. Our study p...

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Autores principales: Wei, Wei, Wei, Xuan, Xie, Xin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Tehran University of Medical Sciences 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10362831/
https://www.ncbi.nlm.nih.gov/pubmed/37484148
http://dx.doi.org/10.18502/ijph.v52i6.12959
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author Wei, Wei
Wei, Xuan
Xie, Xin
author_facet Wei, Wei
Wei, Xuan
Xie, Xin
author_sort Wei, Wei
collection PubMed
description BACKGROUND: Esophageal squamous cell carcinoma (ESCC), a widely known esophageal disease, severely affects people’s health. Numerous investigations demonstrated that long non-coding RNAs (lncRNAs) performed key jobs inside a wide scope of organic cycles and stand out in malignant growth. Our study planned to investigate the roles and mechanisms of linc01614 in ESCC. METHODS: A Total of 60 ESCC tissue samples including 30 patients with cisplatin sensitivity and 30 patients with cisplatin resistance, who received DDP-based treatment, were obtained from Zhuhai People’s Hospital, Zhuhai City during 2021. These tissues were frozen and saved in a −80 °C ultra-low temperature freezer. We performed CCK-8, clone formation, flow cytometry assays to determine the effect of linc01614 on ESCC progression, and explored the specific mechanism of linc01614 in ESCC cell proliferation, apoptosis, and chemotherapy resistance. RESULTS: linc01614 expression was upregulated in ESCC tissues and cells compared with non-tumor tissues and human normal esophageal epithelial cells (Het-1A). Knockdown of linc01614 repressed cell expansion, chemotherapy opposition, and advanced cell apoptosis in ESCC. Besides, linc01614 regulated the expression of miR-4775 as a competitive endogenous RNA (ceRNA). CONCLUSION: The linc01614/miR-4775 axis played an important role in ESCC progression and drug resistance, revealing that linc01614 is a promising target in ESCC treatment.
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spelling pubmed-103628312023-07-23 Linc01614 Regulates the Proliferation, Apoptosis, and Chemotherapy Resistance in Esophageal Squamous Cell Carcinoma by Targeting Mir-4775 Wei, Wei Wei, Xuan Xie, Xin Iran J Public Health Original Article BACKGROUND: Esophageal squamous cell carcinoma (ESCC), a widely known esophageal disease, severely affects people’s health. Numerous investigations demonstrated that long non-coding RNAs (lncRNAs) performed key jobs inside a wide scope of organic cycles and stand out in malignant growth. Our study planned to investigate the roles and mechanisms of linc01614 in ESCC. METHODS: A Total of 60 ESCC tissue samples including 30 patients with cisplatin sensitivity and 30 patients with cisplatin resistance, who received DDP-based treatment, were obtained from Zhuhai People’s Hospital, Zhuhai City during 2021. These tissues were frozen and saved in a −80 °C ultra-low temperature freezer. We performed CCK-8, clone formation, flow cytometry assays to determine the effect of linc01614 on ESCC progression, and explored the specific mechanism of linc01614 in ESCC cell proliferation, apoptosis, and chemotherapy resistance. RESULTS: linc01614 expression was upregulated in ESCC tissues and cells compared with non-tumor tissues and human normal esophageal epithelial cells (Het-1A). Knockdown of linc01614 repressed cell expansion, chemotherapy opposition, and advanced cell apoptosis in ESCC. Besides, linc01614 regulated the expression of miR-4775 as a competitive endogenous RNA (ceRNA). CONCLUSION: The linc01614/miR-4775 axis played an important role in ESCC progression and drug resistance, revealing that linc01614 is a promising target in ESCC treatment. Tehran University of Medical Sciences 2023-06 /pmc/articles/PMC10362831/ /pubmed/37484148 http://dx.doi.org/10.18502/ijph.v52i6.12959 Text en Copyright © 2023 Wei et al. Published by Tehran University of Medical Sciences https://creativecommons.org/licenses/by-nc/4.0/This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International license (https://creativecommons.org/licenses/by-nc/4.0/). Non-commercial uses of the work are permitted, provided the original work is properly cited.
spellingShingle Original Article
Wei, Wei
Wei, Xuan
Xie, Xin
Linc01614 Regulates the Proliferation, Apoptosis, and Chemotherapy Resistance in Esophageal Squamous Cell Carcinoma by Targeting Mir-4775
title Linc01614 Regulates the Proliferation, Apoptosis, and Chemotherapy Resistance in Esophageal Squamous Cell Carcinoma by Targeting Mir-4775
title_full Linc01614 Regulates the Proliferation, Apoptosis, and Chemotherapy Resistance in Esophageal Squamous Cell Carcinoma by Targeting Mir-4775
title_fullStr Linc01614 Regulates the Proliferation, Apoptosis, and Chemotherapy Resistance in Esophageal Squamous Cell Carcinoma by Targeting Mir-4775
title_full_unstemmed Linc01614 Regulates the Proliferation, Apoptosis, and Chemotherapy Resistance in Esophageal Squamous Cell Carcinoma by Targeting Mir-4775
title_short Linc01614 Regulates the Proliferation, Apoptosis, and Chemotherapy Resistance in Esophageal Squamous Cell Carcinoma by Targeting Mir-4775
title_sort linc01614 regulates the proliferation, apoptosis, and chemotherapy resistance in esophageal squamous cell carcinoma by targeting mir-4775
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10362831/
https://www.ncbi.nlm.nih.gov/pubmed/37484148
http://dx.doi.org/10.18502/ijph.v52i6.12959
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AT xiexin linc01614regulatestheproliferationapoptosisandchemotherapyresistanceinesophagealsquamouscellcarcinomabytargetingmir4775