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Abstract：
BACKGROUND: Long non-coding RNA (lncRNA) is a group of RNA transcripts that contribute to tumor development by post-transcriptionally regulating cancer-related genes. Nasopharyngeal carcinoma (NPC) is an epithelial tumor that occurs in the nasopharynx and is common in North Africa and Southeast Asia. The study investigated the functions of lncRNA TMPO-AS1 in NPC cell proliferation and apoptosis as well as its related competing endogenous RNA (ceRNA) mechanism.
METHODS: Candidate microRNA and genes that may regulated by TMPO-AS1 were predicted with the bioinformatic tool starBase. TMPO-AS1 expression in NPC tissue, cells, nuclear part, and cytoplasmic part was measured by RT-qPCR. MTT assay, EdU assay, and flow cytometry analysis were carried out to evaluate NPC cell viability, proliferation, and apoptosis, respectively. RNA immunoprecipitation assay and luciferase reporter assay were conducted to detect the binding between TMPO-AS1 and let-7c-5p or that between let-7c-5p and BCAT1.
RESULTS: TMPO-AS1 and BCAT1 showed high expression in NPC tissue and cells, while let-7c-5p was downregulated in NPC. The silencing of TMPO-AS1 suppressed NPC cell proliferation while promoting cell apoptosis. Moreover, TMPO-AS1 interacted with let-7c-5p and negatively regulated let-7c-5p expression. BCAT1 was a target of let-7c-5p and was inversely regulated by let-7c-5p in NPC cells. The repressive impact of TMPO-AS1 knockdown on NPC cell growth was countervailed by overexpressed BCAT1.
CONCLUSIONS: TMPO-AS1 accelerates NPC cell proliferation and represses cell apoptosis by interacting with let-7c-5p to regulate BCAT1 expression.
METHODS: Candidate microRNA and genes that may regulated by TMPO-AS1 were predicted with the bioinformatic tool starBase. TMPO-AS1 expression in NPC tissue, cells, nuclear part, and cytoplasmic part was measured by RT-qPCR. MTT assay, EdU assay, and flow cytometry analysis were carried out to evaluate NPC cell viability, proliferation, and apoptosis, respectively. RNA immunoprecipitation assay and luciferase reporter assay were conducted to detect the binding between TMPO-AS1 and let-7c-5p or that between let-7c-5p and BCAT1.
RESULTS: TMPO-AS1 and BCAT1 showed high expression in NPC tissue and cells, while let-7c-5p was downregulated in NPC. The silencing of TMPO-AS1 suppressed NPC cell proliferation while promoting cell apoptosis. Moreover, TMPO-AS1 interacted with let-7c-5p and negatively regulated let-7c-5p expression. BCAT1 was a target of let-7c-5p and was inversely regulated by let-7c-5p in NPC cells. The repressive impact of TMPO-AS1 knockdown on NPC cell growth was countervailed by overexpressed BCAT1.
CONCLUSIONS: TMPO-AS1 accelerates NPC cell proliferation and represses cell apoptosis by interacting with let-7c-5p to regulate BCAT1 expression.
摘要：
背景：长非编码RNA（lncRNA）是一组通过转录后调节癌症相关基因而促进肿瘤发展的RNA转录本。鼻咽癌（NPC）是一种发生在鼻咽部的上皮性肿瘤，常见于北非和东南亚。本研究探讨了lncRNATMPO-AS1在鼻咽癌细胞增殖和凋亡中的功能及其相关的竞争性内源性RNA(ceRNA)机制。
方法：用生物信息学工具starBase预测可能受TMPO-AS1调控的候选microRNA和基因。TMPO-AS1在鼻咽癌组织中的表达,细胞,核部分,通过RT-qPCR测量细胞质部分。MTT测定，EdU分析，和流式细胞术分析进行评估NPC细胞的活力，扩散,和细胞凋亡，分别。进行RNA免疫沉淀测定和荧光素酶报告基因测定以检测TMPO-AS1与let-7c-5p之间或let-7c-5p与BCATl之间的结合。
结果：TMPO-AS1和BCAT1在NPC组织和细胞中呈高表达，而let-7c-5p在鼻咽癌中下调。沉默TMPO-AS1抑制NPC细胞增殖，同时促进细胞凋亡。此外，TMPO-AS1与let-7c-5p相互作用，并负调控let-7c-5p的表达。BCATl是let-7c-5p的靶标,并且在NPC细胞中被let-7c-5p反向调节。过表达的BCAT1抵消了TMPO-AS1敲低对NPC细胞生长的抑制作用。
结论：TMPO-AS1通过与let-7c-5p相互作用调节BCAT1表达，加速NPC细胞增殖并抑制细胞凋亡。
方法：用生物信息学工具starBase预测可能受TMPO-AS1调控的候选microRNA和基因。TMPO-AS1在鼻咽癌组织中的表达,细胞,核部分,通过RT-qPCR测量细胞质部分。MTT测定，EdU分析，和流式细胞术分析进行评估NPC细胞的活力，扩散,和细胞凋亡，分别。进行RNA免疫沉淀测定和荧光素酶报告基因测定以检测TMPO-AS1与let-7c-5p之间或let-7c-5p与BCATl之间的结合。
结果：TMPO-AS1和BCAT1在NPC组织和细胞中呈高表达，而let-7c-5p在鼻咽癌中下调。沉默TMPO-AS1抑制NPC细胞增殖，同时促进细胞凋亡。此外，TMPO-AS1与let-7c-5p相互作用，并负调控let-7c-5p的表达。BCATl是let-7c-5p的靶标,并且在NPC细胞中被let-7c-5p反向调节。过表达的BCAT1抵消了TMPO-AS1敲低对NPC细胞生长的抑制作用。
结论：TMPO-AS1通过与let-7c-5p相互作用调节BCAT1表达，加速NPC细胞增殖并抑制细胞凋亡。
