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MiR-1193 Inhibits the Malignancy of Cervical Cancer Cells by Targeting Claudin 7 (CLDN7)

OBJECTIVE: MicroRNAs (miRNAs) are highly involved in cancer development, including in cervical cancer (CC). In this study, we aimed to investigate the role and possible mechanism of a poorly studied miRNA, miR-1193, in CC progression. MATERIALS AND METHODS: Expression of miR-1193 was determined in 6...

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Autores principales: Zhang, Bin, Lin, Yao, Bao, Qiufang, Zheng, Yantong, Lan, Lan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7245469/
https://www.ncbi.nlm.nih.gov/pubmed/32547067
http://dx.doi.org/10.2147/OTT.S247115
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author Zhang, Bin
Lin, Yao
Bao, Qiufang
Zheng, Yantong
Lan, Lan
author_facet Zhang, Bin
Lin, Yao
Bao, Qiufang
Zheng, Yantong
Lan, Lan
author_sort Zhang, Bin
collection PubMed
description OBJECTIVE: MicroRNAs (miRNAs) are highly involved in cancer development, including in cervical cancer (CC). In this study, we aimed to investigate the role and possible mechanism of a poorly studied miRNA, miR-1193, in CC progression. MATERIALS AND METHODS: Expression of miR-1193 was determined in 60 pairs of cervical samples. The impacts of miR-1193 on CC cell proliferation, invasion and migration capacities were verified by CCK-8, transwell and wound healing assays, respectively. Then, bioinformatics prediction, luciferase reporter assay, qRT-PCR and Western blot were successively conducted to study the targeting of claudin 7 (CLDN7) by miR-1193. After CLDN7 was restored in miR-1193-overexpressed cells, the rescue effects were determined. Finally, CLDN7 expression was analyzed in cervical samples, and its expression correlation with miR-1193 was explored. RESULTS: Compared with paired normal tissues, miR-1193 was sharply decreased in abnormal tissues (intraepithelial lesions and cancerous tissues). Especially, miR-1193 expression was gradually decreased in low-grade squamous intraepithelial lesions, high-grade squamous intraepithelial lesions and CC. Enforced expression of miR-1193 inhibited CC cell proliferation, invasion and migration. Mechanistically, we confirmed CLDN7 as a target of miR-1193, and restoration of CLDN7 robustly rescued the tumor suppressing effects of miR-1193 in CC cells. CLDN7 was upregulated in abnormal cervical tissues and its expression exhibited inverse correlation with that of miR-1193 in CC. CONCLUSION: Our results suggested that miR-1193 exerted tumor inhibitory roles in CC malignancy by directly targeting CLDN7.
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spelling pubmed-72454692020-06-15 MiR-1193 Inhibits the Malignancy of Cervical Cancer Cells by Targeting Claudin 7 (CLDN7) Zhang, Bin Lin, Yao Bao, Qiufang Zheng, Yantong Lan, Lan Onco Targets Ther Original Research OBJECTIVE: MicroRNAs (miRNAs) are highly involved in cancer development, including in cervical cancer (CC). In this study, we aimed to investigate the role and possible mechanism of a poorly studied miRNA, miR-1193, in CC progression. MATERIALS AND METHODS: Expression of miR-1193 was determined in 60 pairs of cervical samples. The impacts of miR-1193 on CC cell proliferation, invasion and migration capacities were verified by CCK-8, transwell and wound healing assays, respectively. Then, bioinformatics prediction, luciferase reporter assay, qRT-PCR and Western blot were successively conducted to study the targeting of claudin 7 (CLDN7) by miR-1193. After CLDN7 was restored in miR-1193-overexpressed cells, the rescue effects were determined. Finally, CLDN7 expression was analyzed in cervical samples, and its expression correlation with miR-1193 was explored. RESULTS: Compared with paired normal tissues, miR-1193 was sharply decreased in abnormal tissues (intraepithelial lesions and cancerous tissues). Especially, miR-1193 expression was gradually decreased in low-grade squamous intraepithelial lesions, high-grade squamous intraepithelial lesions and CC. Enforced expression of miR-1193 inhibited CC cell proliferation, invasion and migration. Mechanistically, we confirmed CLDN7 as a target of miR-1193, and restoration of CLDN7 robustly rescued the tumor suppressing effects of miR-1193 in CC cells. CLDN7 was upregulated in abnormal cervical tissues and its expression exhibited inverse correlation with that of miR-1193 in CC. CONCLUSION: Our results suggested that miR-1193 exerted tumor inhibitory roles in CC malignancy by directly targeting CLDN7. Dove 2020-05-19 /pmc/articles/PMC7245469/ /pubmed/32547067 http://dx.doi.org/10.2147/OTT.S247115 Text en © 2020 Zhang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Zhang, Bin
Lin, Yao
Bao, Qiufang
Zheng, Yantong
Lan, Lan
MiR-1193 Inhibits the Malignancy of Cervical Cancer Cells by Targeting Claudin 7 (CLDN7)
title MiR-1193 Inhibits the Malignancy of Cervical Cancer Cells by Targeting Claudin 7 (CLDN7)
title_full MiR-1193 Inhibits the Malignancy of Cervical Cancer Cells by Targeting Claudin 7 (CLDN7)
title_fullStr MiR-1193 Inhibits the Malignancy of Cervical Cancer Cells by Targeting Claudin 7 (CLDN7)
title_full_unstemmed MiR-1193 Inhibits the Malignancy of Cervical Cancer Cells by Targeting Claudin 7 (CLDN7)
title_short MiR-1193 Inhibits the Malignancy of Cervical Cancer Cells by Targeting Claudin 7 (CLDN7)
title_sort mir-1193 inhibits the malignancy of cervical cancer cells by targeting claudin 7 (cldn7)
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7245469/
https://www.ncbi.nlm.nih.gov/pubmed/32547067
http://dx.doi.org/10.2147/OTT.S247115
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