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Abstract：
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: CircBFAR, miR-31-5p, and COL5A1 in LSCC progression might provide novel therapeutic targets for LSCC clinical intervention.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: CircBFAR, miR-31-5p, and COL5A1 in LSCC progression might provide novel therapeutic targets for LSCC clinical intervention.
摘要：
UNASSIGNED：喉鳞状细胞癌（LSCC）是起源于呼吸系统的高度恶性肿瘤。环状RNA已被报道与多种癌症的治疗和预后有关。包括LSCC。
未经批准：circBFAR的表达，miR-31-5p,通过定量实时聚合酶链反应检测LSCC组织和细胞中的V型胶原α1链（COL5A1）。细胞计数试剂盒8和5-乙炔基-2'-脱氧尿苷测定法用于检测细胞增殖。伤口愈合试验和transwell试验用于测试细胞迁移和侵袭，分别。用westernblot检测LSCC细胞中的蛋白表达。miR-31-5p与circBFAR或COL5A1之间的关系通过双荧光素酶报告基因测定进行鉴定,RNA下拉法,和免疫沉淀测定。通过肿瘤异种移植小鼠实验检测circbfar对体内肿瘤生长的影响。免疫组化法检测LSCC组织中COL5A1和KI-67的蛋白表达。
未经证实：CircBFAR在LSCC组织和细胞中增加，并且与LSCC患者的晚期临床分期和总生存期相关。通过circBFAR敲低和沉默circBFAR阻断LSCC细胞的迁移和侵袭来抑制细胞活力和增殖。CircBFAR敲低抑制了细胞管形成，以及KI-67，基质金属肽酶2（MMP2）的蛋白表达，和血管内皮生长因子A（VEGFA）在LSCC细胞。MiR-31-5p是大约BFAR的目标，和circBFAR缺乏对生存力的抑制作用，扩散,迁移,入侵,通过miR-31-5p下调来挽救LSCC细胞中的管形成和KI-67，MMP2和VEGFA的蛋白表达。COL5A1受miR-31-5p负调控,并在LSCC组织和细胞中增强。COL5A1过表达逆转了miR-31-5p对LSCC细胞的抑制作用。CircBFAR不足阻碍了体内肿瘤的生长。
未经批准：CircBFAR，miR-31-5p,LSCC进展中的COL5A1可能为LSCC临床干预提供新的治疗靶点。
未经批准：circBFAR的表达，miR-31-5p,通过定量实时聚合酶链反应检测LSCC组织和细胞中的V型胶原α1链（COL5A1）。细胞计数试剂盒8和5-乙炔基-2'-脱氧尿苷测定法用于检测细胞增殖。伤口愈合试验和transwell试验用于测试细胞迁移和侵袭，分别。用westernblot检测LSCC细胞中的蛋白表达。miR-31-5p与circBFAR或COL5A1之间的关系通过双荧光素酶报告基因测定进行鉴定,RNA下拉法,和免疫沉淀测定。通过肿瘤异种移植小鼠实验检测circbfar对体内肿瘤生长的影响。免疫组化法检测LSCC组织中COL5A1和KI-67的蛋白表达。
未经证实：CircBFAR在LSCC组织和细胞中增加，并且与LSCC患者的晚期临床分期和总生存期相关。通过circBFAR敲低和沉默circBFAR阻断LSCC细胞的迁移和侵袭来抑制细胞活力和增殖。CircBFAR敲低抑制了细胞管形成，以及KI-67，基质金属肽酶2（MMP2）的蛋白表达，和血管内皮生长因子A（VEGFA）在LSCC细胞。MiR-31-5p是大约BFAR的目标，和circBFAR缺乏对生存力的抑制作用，扩散,迁移,入侵,通过miR-31-5p下调来挽救LSCC细胞中的管形成和KI-67，MMP2和VEGFA的蛋白表达。COL5A1受miR-31-5p负调控,并在LSCC组织和细胞中增强。COL5A1过表达逆转了miR-31-5p对LSCC细胞的抑制作用。CircBFAR不足阻碍了体内肿瘤的生长。
未经批准：CircBFAR，miR-31-5p,LSCC进展中的COL5A1可能为LSCC临床干预提供新的治疗靶点。
