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Abstract：
UNASSIGNED: Gastric cancer (GC) is the leading digestive malignancy with high incidence and mortality rate. microRNAs (miRs) play an important role in GC progresssion. This study aimed to investigate the effect of miR-98-5p on proliferation, migration, and invasion of GC cells.
UNASSIGNED: The expression levels of miR-98-5p, ubiquitin specific peptidase 44 (USP44), and CCCTCbinding factor-like (CTCFL) in GC tissues and cells were identified using reversetranscription quantitative polymerase chain reaction and Western blot assay. The relationship between miR-98-5p expression/USP44 and the clinicopathological features in GC patients was analyzed. GC cell proliferation, invasion, and migration were evaluated by cell counting kit-8 and clone formation assays and Transwell assays. The bindings of miR-98-5p to USP44 and USP44 to CTCFL were examined using dualluciferase assay and co-immunoprecipitation. GC cells were treated with MG132 and the ubiquitination level of CTCFL was examined using ubiquitination assay. Rescue experiments were performed to verify the roles of USP44 and CTCFL in GC cells.
UNASSIGNED: miR-98-5p was downregulated in GC. miR-98-5p overexpression inhibited the proliferation, migration, and invasion of GC cells. miR-98-5p inhibited USP44 expression. USP44 bound to CTCFL and limited ubiquitination degradation of CTCFL. Overexpression of USP44 and CTCFL attenuated the inhibitory effects of miR-98-5p overexpression on GC cell progression.
UNASSIGNED: miR-98-5p overexpression limited USP44-mediated CTCFL deubiquitination, and suppressed CTCFL expression, mitigating GC cell proliferation, migration, and invasion.
UNASSIGNED: The expression levels of miR-98-5p, ubiquitin specific peptidase 44 (USP44), and CCCTCbinding factor-like (CTCFL) in GC tissues and cells were identified using reversetranscription quantitative polymerase chain reaction and Western blot assay. The relationship between miR-98-5p expression/USP44 and the clinicopathological features in GC patients was analyzed. GC cell proliferation, invasion, and migration were evaluated by cell counting kit-8 and clone formation assays and Transwell assays. The bindings of miR-98-5p to USP44 and USP44 to CTCFL were examined using dualluciferase assay and co-immunoprecipitation. GC cells were treated with MG132 and the ubiquitination level of CTCFL was examined using ubiquitination assay. Rescue experiments were performed to verify the roles of USP44 and CTCFL in GC cells.
UNASSIGNED: miR-98-5p was downregulated in GC. miR-98-5p overexpression inhibited the proliferation, migration, and invasion of GC cells. miR-98-5p inhibited USP44 expression. USP44 bound to CTCFL and limited ubiquitination degradation of CTCFL. Overexpression of USP44 and CTCFL attenuated the inhibitory effects of miR-98-5p overexpression on GC cell progression.
UNASSIGNED: miR-98-5p overexpression limited USP44-mediated CTCFL deubiquitination, and suppressed CTCFL expression, mitigating GC cell proliferation, migration, and invasion.
摘要：
■胃癌（GC）是主要的消化系统恶性肿瘤，发病率和死亡率都很高。microRNAs(miRs)在GC进展中起重要作用。本研究旨在探讨miR-98-5p对细胞增殖的影响,迁移,和GC细胞的侵袭。
■miR-98-5p的表达水平,泛素特异性肽酶44（USP44），使用逆转录定量聚合酶链反应和Westernblot分析鉴定GC组织和细胞中的CCCTC结合因子样（CTCFL）。分析miR-98-5p表达/USP44与GC患者临床病理特征的关系。GC细胞增殖，入侵,通过细胞计数试剂盒-8和克隆形成测定和Transwell测定评估和迁移。miR-98-5p与USP44的结合和USP44与CTCFL的结合使用双胶凝酶测定和共免疫沉淀进行检查。用MG132处理GC细胞,并使用泛素化测定法检查CTCFL的泛素化水平。进行了挽救实验以验证USP44和CTCFL在GC细胞中的作用。
■miR-98-5p在GC中下调。miR-98-5p过表达抑制细胞增殖,迁移,和GC细胞的侵袭。miR-98-5p抑制USP44表达。USP44结合CTCFL并限制CTCFL的泛素化降解。USP44和CTCFL的过表达减弱了miR-98-5p过表达对GC细胞进展的抑制作用。
■miR-98-5p过表达限制USP44介导的CTCFL去泛素化，并抑制CTCFL表达，减轻GC细胞增殖，迁移,和入侵。
■miR-98-5p的表达水平,泛素特异性肽酶44（USP44），使用逆转录定量聚合酶链反应和Westernblot分析鉴定GC组织和细胞中的CCCTC结合因子样（CTCFL）。分析miR-98-5p表达/USP44与GC患者临床病理特征的关系。GC细胞增殖，入侵,通过细胞计数试剂盒-8和克隆形成测定和Transwell测定评估和迁移。miR-98-5p与USP44的结合和USP44与CTCFL的结合使用双胶凝酶测定和共免疫沉淀进行检查。用MG132处理GC细胞,并使用泛素化测定法检查CTCFL的泛素化水平。进行了挽救实验以验证USP44和CTCFL在GC细胞中的作用。
■miR-98-5p在GC中下调。miR-98-5p过表达抑制细胞增殖,迁移,和GC细胞的侵袭。miR-98-5p抑制USP44表达。USP44结合CTCFL并限制CTCFL的泛素化降解。USP44和CTCFL的过表达减弱了miR-98-5p过表达对GC细胞进展的抑制作用。
■miR-98-5p过表达限制USP44介导的CTCFL去泛素化，并抑制CTCFL表达，减轻GC细胞增殖，迁移,和入侵。
