PMID- 36544920 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20221223 IS - 2378-8038 (Print) IS - 2378-8038 (Electronic) IS - 2378-8038 (Linking) VI - 7 IP - 6 DP - 2022 Dec TI - CircBFAR correlates with poor prognosis and promotes laryngeal squamous cell cancer progression through miR-31-5p/COL5A1 axis. PG - 1951-1962 LID - 10.1002/lio2.966 [doi] AB - INTRODUCTION: Laryngeal squamous cell cancer (LSCC) is a highly malignant tumor originating from the respiratory system. Circular RNAs have been reported to be associated with the treatment and prognosis of a variety of cancers, including LSCC. METHODS: The expression of circBFAR, miR-31-5p, and collagen type V alpha 1 chain (COL5A1) in LSCC tissues and cells was detected by quantitative real-time polymerase chain reaction. Cell counting kit 8 and 5-Ethynyl-2'-deoxyuridine assays were used to detect cell proliferation. Wound healing assay and transwell assay were used to test cell migration and invasion, respectively. The protein expression in LSCC cells was detected with western blot. The relationships between miR-31-5p and circBFAR or COL5A1 were identified by dual-luciferase reporter assay, RNA-pull down assay, and immunoprecipitation assay. The effect of circBFAR on tumor growth in vivo was detected by tumor xenograft mice experiment. The protein expression of COL5A1 and KI-67 in LSCC tissues was measured by immunohistochemistry assay. RESULTS: CircBFAR was increased in LSCC tissues and cells, and was related to advanced clinical stage and overall survival of LSCC patients. The cell viability and proliferation were inhibited by circBFAR knockdown and silencing of circBFAR blocked migration and invasion of LSCC cells. CircBFAR knockdown suppressed cell tube formation, and the protein expression of KI-67, matrix metallopeptidase 2 (MMP2), and vascular endothelial growth factor A (VEGFA) in LSCC cells. MiR-31-5p was the target of circBFAR, and the inhibitory effects of circBFAR deficiency on viability, proliferation, migration, invasion, tube formation and the protein expression of KI-67, MMP2, and VEGFA in LSCC cells were rescued by miR-31-5p downregulation. COL5A1 was negatively regulated by miR-31-5p, and was boosted in LSCC tissues and cells. COL5A1 overexpression reversed the inhibitory effects of miR-31-5p on LSCC cells. CircBFAR insufficiency hindered tumor growth in vivo. CONCLUSION: CircBFAR, miR-31-5p, and COL5A1 in LSCC progression might provide novel therapeutic targets for LSCC clinical intervention. CI - (c) 2022 The Authors. Laryngoscope Investigative Otolaryngology published by Wiley Periodicals LLC on behalf of The Triological Society. FAU - Gong, Hengcui AU - Gong H AD - Department of Otolaryngology Yibin Hospital of Traditional Chinese Medicine Yibin Sichuan China. FAU - Wu, Wei AU - Wu W AD - Department of Radiotherapy GanZhou Cancer Hospital/The Affiliated Cancer Hospital of Gannan Medical University GanZhou Jiangxi China. FAU - Fang, Chuankai AU - Fang C AD - Department of Ophthalmology Tongxiang First people's Hospital Tongxiang Zhejiang China. FAU - He, Di AU - He D AUID- ORCID: 0000-0002-8927-4555 AD - Department of Otorhinolaryngology Tongxiang First people's Hospital Tongxiang Zhejiang China. LA - eng PT - Journal Article DEP - 20221103 PL - United States TA - Laryngoscope Investig Otolaryngol JT - Laryngoscope investigative otolaryngology JID - 101684963 PMC - PMC9764770 OTO - NOTNLM OT - COL5A1 OT - CircBFAR OT - laryngeal squamous cell cancer OT - miR-31-5p COIS- The author declares that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported. EDAT- 2022/12/23 06:00 MHDA- 2022/12/23 06:01 PMCR- 2022/11/03 CRDT- 2022/12/22 02:26 PHST- 2022/01/24 00:00 [received] PHST- 2022/06/27 00:00 [revised] PHST- 2022/07/21 00:00 [accepted] PHST- 2022/12/22 02:26 [entrez] PHST- 2022/12/23 06:00 [pubmed] PHST- 2022/12/23 06:01 [medline] PHST- 2022/11/03 00:00 [pmc-release] AID - LIO2966 [pii] AID - 10.1002/lio2.966 [doi] PST - epublish SO - Laryngoscope Investig Otolaryngol. 2022 Nov 3;7(6):1951-1962. doi: 10.1002/lio2.966. eCollection 2022 Dec.