MicroRNA-145-5p modulates Krüppel-like factor 5 and inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma
Abstract Background In several human cancers, Krüppel-like factor 5 (KLF5), a zinc finger transcription factor, can contribute to both tumor progression or suppression; however, the precise role of KLF5 in nasopharyngeal carcinoma (NPC) remains poorly understood. In this study, the association betwe...
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BMC
2022-07-01
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Online Access: | https://doi.org/10.1186/s12860-022-00430-9 |
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author | Chien-Han Yuan Wei-Chi Hsu A.-Mei Huang Ben-Chih Yuan I.-Hung Chen Chia-An Hsu Rong-Feng Chen Yih-Min Chu Hui-Hui Lin Hung-Lung Ke |
author_facet | Chien-Han Yuan Wei-Chi Hsu A.-Mei Huang Ben-Chih Yuan I.-Hung Chen Chia-An Hsu Rong-Feng Chen Yih-Min Chu Hui-Hui Lin Hung-Lung Ke |
author_sort | Chien-Han Yuan |
collection | DOAJ |
description | Abstract Background In several human cancers, Krüppel-like factor 5 (KLF5), a zinc finger transcription factor, can contribute to both tumor progression or suppression; however, the precise role of KLF5 in nasopharyngeal carcinoma (NPC) remains poorly understood. In this study, the association between KLF5 and microRNA-145-5p (miR-145-5p) in NPC cells was elucidated. Results Our results showed that KLF5 expression was up-regulated in NPC group compared to normal group. We found that KLF5 exhibited an oncogenic role in NPC cells. The upregulation of miR-145-5p inhibited the proliferation, migration, and invasion of NPC cells. It was observed that miR-145-5p could down-regulate the mRNA and protein expression of KLF5 in NPC cell lines. Additionally, the activity of focal adhesion kinase (FAK), a migration marker, was regulated by miR-145-5p and KLF5 in NPC cells. Conclusions The results of this study indicated that miR-145-5p could repress the proliferation, migration, and invasion of NPC cells via KLF5/FAK regulation, and could be a potential therapeutic target for patients with NPC. |
first_indexed | 2024-12-11T01:00:09Z |
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id | doaj.art-82af62d2afc945eb9412c5914696f268 |
institution | Directory Open Access Journal |
issn | 2661-8850 |
language | English |
last_indexed | 2024-12-11T01:00:09Z |
publishDate | 2022-07-01 |
publisher | BMC |
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spelling | doaj.art-82af62d2afc945eb9412c5914696f2682022-12-22T01:26:21ZengBMCBMC Molecular and Cell Biology2661-88502022-07-0123111410.1186/s12860-022-00430-9MicroRNA-145-5p modulates Krüppel-like factor 5 and inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinomaChien-Han Yuan0Wei-Chi Hsu1A.-Mei Huang2Ben-Chih Yuan3I.-Hung Chen4Chia-An Hsu5Rong-Feng Chen6Yih-Min Chu7Hui-Hui Lin8Hung-Lung Ke9Department of Otolaryngology, Kaohsiung Armed Forces General HospitalDepartment of Urology, School of Medicine, College of Medicine, Kaohsiung Medical UniversityGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical UniversityDepartment of Otolaryngology, Fooyin University HospitalDepartment of Internal Medicine, Pingtung Branch, Kaohsiung Armed Forces General HospitalDepartment of Otolaryngology, Kaohsiung Armed Forces General HospitalDepartment of Otolaryngology, Kaohsiung Armed Forces General HospitalDepartment of Otolaryngology, Kaohsiung Armed Forces General HospitalDepartment of Urology, Kaohsiung Medical University Hospital, Kaohsiung Medical UniversityDepartment of Urology, School of Medicine, College of Medicine, Kaohsiung Medical UniversityAbstract Background In several human cancers, Krüppel-like factor 5 (KLF5), a zinc finger transcription factor, can contribute to both tumor progression or suppression; however, the precise role of KLF5 in nasopharyngeal carcinoma (NPC) remains poorly understood. In this study, the association between KLF5 and microRNA-145-5p (miR-145-5p) in NPC cells was elucidated. Results Our results showed that KLF5 expression was up-regulated in NPC group compared to normal group. We found that KLF5 exhibited an oncogenic role in NPC cells. The upregulation of miR-145-5p inhibited the proliferation, migration, and invasion of NPC cells. It was observed that miR-145-5p could down-regulate the mRNA and protein expression of KLF5 in NPC cell lines. Additionally, the activity of focal adhesion kinase (FAK), a migration marker, was regulated by miR-145-5p and KLF5 in NPC cells. Conclusions The results of this study indicated that miR-145-5p could repress the proliferation, migration, and invasion of NPC cells via KLF5/FAK regulation, and could be a potential therapeutic target for patients with NPC.https://doi.org/10.1186/s12860-022-00430-9Nasopharyngeal carcinomaMicroRNA-145-5pKrüppel-like factor 5Focal adhesion kinaseCell migrationCell invasion |
spellingShingle | Chien-Han Yuan Wei-Chi Hsu A.-Mei Huang Ben-Chih Yuan I.-Hung Chen Chia-An Hsu Rong-Feng Chen Yih-Min Chu Hui-Hui Lin Hung-Lung Ke MicroRNA-145-5p modulates Krüppel-like factor 5 and inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma BMC Molecular and Cell Biology Nasopharyngeal carcinoma MicroRNA-145-5p Krüppel-like factor 5 Focal adhesion kinase Cell migration Cell invasion |
title | MicroRNA-145-5p modulates Krüppel-like factor 5 and inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma |
title_full | MicroRNA-145-5p modulates Krüppel-like factor 5 and inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma |
title_fullStr | MicroRNA-145-5p modulates Krüppel-like factor 5 and inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma |
title_full_unstemmed | MicroRNA-145-5p modulates Krüppel-like factor 5 and inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma |
title_short | MicroRNA-145-5p modulates Krüppel-like factor 5 and inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma |
title_sort | microrna 145 5p modulates kruppel like factor 5 and inhibits cell proliferation migration and invasion in nasopharyngeal carcinoma |
topic | Nasopharyngeal carcinoma MicroRNA-145-5p Krüppel-like factor 5 Focal adhesion kinase Cell migration Cell invasion |
url | https://doi.org/10.1186/s12860-022-00430-9 |
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