PDF(Pubmed)
Abstract：
UNASSIGNED: Esophageal squamous cell carcinoma (ESCC) is a malignancy usually associated with smoking or alcohol consumption. The involvement of long noncoding RNAs (lncRNAs) in the regulation of tumor development and metastasis through molecular mechanisms has been unveiled by accumulating evidence. However, the function of lncRNA SUMO1 Pseudogene 3 (lncSUMO1P3) essential to ESCC development remains obscure.
UNASSIGNED: Reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) and Western blot (WB) analysis were done to measure RNA and protein levels. Functional assays were carried out to examine the changes in ESCC cell phenotype. Supported by bioinformatics analysis, mechanism assays were done for assessment of putative interactions among different genes.
UNASSIGNED: LlncSUMO1P3 was aberrantly up-regulated in ESCC cell lines, and lncSUMO1P3 deficiency could hamper cell proliferation, migration and invasion as well as epithelial-mesenchymaltransition (EMT) in ESCC while lncSUMO1P3 overexpression led to the opposite consequences. LncSUMO1P3 could competitively bind to microRNA-486-5p (miR-486-5p) or PHD finger protein 8 (PHF8) to modulate CD151 expression. CD151 was also verified to regulate ESCC cell biological behaviors.
UNASSIGNED: Our study revealed that lncSUMO1P3, up-regulated in ESCC cells, could sponge miR-486-5p and recruit PHF8 to up-regulate CD151, thus influencing the malignant behaviors of ESCC cells.
UNASSIGNED: Reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) and Western blot (WB) analysis were done to measure RNA and protein levels. Functional assays were carried out to examine the changes in ESCC cell phenotype. Supported by bioinformatics analysis, mechanism assays were done for assessment of putative interactions among different genes.
UNASSIGNED: LlncSUMO1P3 was aberrantly up-regulated in ESCC cell lines, and lncSUMO1P3 deficiency could hamper cell proliferation, migration and invasion as well as epithelial-mesenchymaltransition (EMT) in ESCC while lncSUMO1P3 overexpression led to the opposite consequences. LncSUMO1P3 could competitively bind to microRNA-486-5p (miR-486-5p) or PHD finger protein 8 (PHF8) to modulate CD151 expression. CD151 was also verified to regulate ESCC cell biological behaviors.
UNASSIGNED: Our study revealed that lncSUMO1P3, up-regulated in ESCC cells, could sponge miR-486-5p and recruit PHF8 to up-regulate CD151, thus influencing the malignant behaviors of ESCC cells.
摘要：
■食管鳞状细胞癌（ESCC）是一种恶性肿瘤，通常与吸烟或饮酒有关。越来越多的证据揭示了长链非编码RNA（lncRNA）通过分子机制参与肿瘤发展和转移的调控。然而,lncRNASUMO1假基因3（lncSUMO1P3）对ESCC发展至关重要的功能仍然不清楚。
■进行逆转录定量实时聚合酶链反应（RT-qPCR）和蛋白质印迹（WB）分析以测量RNA和蛋白质水平。进行功能测定以检查ESCC细胞表型的变化。生物信息学分析支持，进行了机制分析，以评估不同基因之间的推定相互作用。
■LlncSUMO1P3在ESCC细胞系中异常上调，lncSUMO1P3缺乏会阻碍细胞增殖，ESCC中的迁移和侵袭以及上皮-间质转化（EMT），而lncSUMO1P3过表达导致相反的后果。LncSUMO1P3可以竞争性结合microRNA-486-5p（miR-486-5p）或PHD指蛋白8（PHF8）以调节CD151表达。CD151也被证实可以调节ESCC细胞的生物学行为。
■我们的研究表明，lncSUMO1P3在ESCC细胞中上调，可以海绵化miR-486-5p并招募PHF8上调CD151，从而影响ESCC细胞的恶性行为。
■进行逆转录定量实时聚合酶链反应（RT-qPCR）和蛋白质印迹（WB）分析以测量RNA和蛋白质水平。进行功能测定以检查ESCC细胞表型的变化。生物信息学分析支持，进行了机制分析，以评估不同基因之间的推定相互作用。
■LlncSUMO1P3在ESCC细胞系中异常上调，lncSUMO1P3缺乏会阻碍细胞增殖，ESCC中的迁移和侵袭以及上皮-间质转化（EMT），而lncSUMO1P3过表达导致相反的后果。LncSUMO1P3可以竞争性结合microRNA-486-5p（miR-486-5p）或PHD指蛋白8（PHF8）以调节CD151表达。CD151也被证实可以调节ESCC细胞的生物学行为。
■我们的研究表明，lncSUMO1P3在ESCC细胞中上调，可以海绵化miR-486-5p并招募PHF8上调CD151，从而影响ESCC细胞的恶性行为。
