Hou Min, Wu Nannan, Yao Lili
Clinical Laboratory, Tianjin Chest Hospital, No. 261, South Taierzhuang Road, Tianjin, 300222, China.
Cancer Cell Int. 2021 Jan 9;21(1):36. doi: 10.1186/s12935-020-01685-y.
Long non-coding RNAs (lncRNAs) are pervasively transcribed in genome and emerging as a new player in tumorigenesis due to their functions in transcriptional, posttranscriptional and epigenetic mechanisms of gene regulation. As the most frequent malignancy and the foremost source of cancer mortality, lung cancer is a heterogeneous disorder. The most common type of lung cancer is Non-small cell lung cancer (NSCLC), occupying 85% of the total cases, and the main subtypes of NSCLC include lung adenocarcinoma (LAD), large cell carcinoma (LCC), and lung squamous cell carcinoma (LSCC). Recently, numerous lncRNAs have been reported to be strongly linked to NSCLC. In the present study, we found that a new lncRNA CBR3-AS1 is highly expressed in lung cancer. In addition, we also examined the expression of lncRNA CBR3-AS1 in 60 of LADs, 40 of LCCs and 40 of LSCCs patient samples, finding that CBR3-AS1 was specificity highly expressed in LAD cancer tissues. Mechanically, we discovered that CBR3-AS1 could regulate the proliferation, migration and invasion of LAD cells through targeting Wnt/β-catenin signaling.
Real-time PCR, RNA-pulldown, RIP, western blotting, lentivirus transfection, luciferase reporter assays, cell proliferation assays, colony formation assays, wound healing scratch assays and transwell assays were employed to examine the relationship between lncRNA CBR3-AS1 and its regulation of Wnt/β-catenin signaling in LAD cells.
LncRNA CBR3-AS1 is highly-expressed in LAD and cell lines. LncRNA CBR3-AS1 shows physical association with β-catenin. CBR3-AS1 could facilitate Wnt/β-catenin signaling activation thought promoting nuclear localization of β-catenin. CBR3-AS1 promotes LAD cell proliferation, migration and invasion by targeting Wnt/β-catenin signaling.
It can be found that a new functional lncRNA CBR3-AS1 could promote nuclear localization of β-catenin so as to facilitate Wnt/β-catenin signaling activation and regulate the proliferation, migration and invasion of LAD cells.
长链非编码RNA（lncRNAs）在基因组中广泛转录，并因其在基因调控的转录、转录后和表观遗传机制中的作用而成为肿瘤发生中的新角色。肺癌作为最常见的恶性肿瘤和癌症死亡的首要原因，是一种异质性疾病。最常见的肺癌类型是非小细胞肺癌（NSCLC），占总病例的85%，NSCLC的主要亚型包括肺腺癌（LAD）、大细胞癌（LCC）和肺鳞状细胞癌（LSCC）。最近，大量lncRNAs被报道与NSCLC密切相关。在本研究中，我们发现一种新的lncRNA CBR3-AS1在肺癌中高表达。此外，我们还检测了lncRNA CBR3-AS1在60例LAD、40例LCC和40例LSCC患者样本中的表达，发现CBR3-AS1在LAD癌组织中特异性高表达。机制上，我们发现CBR3-AS1可通过靶向Wnt/β-连环蛋白信号通路调节LAD细胞的增殖、迁移和侵袭。
采用实时PCR、RNA下拉、RIP、蛋白质免疫印迹、慢病毒转染、荧光素酶报告基因检测、细胞增殖检测、集落形成检测、伤口愈合划痕检测和Transwell检测等方法，研究lncRNA CBR3-AS1与LAD细胞中Wnt/β-连环蛋白信号通路调控之间的关系。
lncRNA CBR3-AS1在LAD及细胞系中高表达。lncRNA CBR3-AS1与β-连环蛋白存在物理相互作用。CBR3-AS1可通过促进β-连环蛋白的核定位来促进Wnt/β-连环蛋白信号通路的激活。CBR3-AS1通过靶向Wnt/β-连环蛋白信号通路促进LAD细胞的增殖、迁移和侵袭。
发现一种新的功能性lncRNA CBR3-AS1可促进β-连环蛋白的核定位，从而促进Wnt/β-连环蛋白信号通路的激活，并调节LAD细胞的增殖、迁移和侵袭。
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