Department of Thoracic surgery, Changzhi People's Hospital, Changzhi, China.
Department of Thoracic surgery, Heji Hospital Affiliated to Changzhi Medical College, Changzhi, China.
J Clin Lab Anal. 2020 Apr;34(4):e23122. doi: 10.1002/jcla.23122. Epub 2019 Nov 19.
The non-small cell lung cancer (NSCLC) is a common malignancy worldwide. Numerous reports have shown the critical role of long non-coding RNAs (lncRNAs) in NSCLC. However, the role of a novel lncRNA named LNBC3 is still unknown.
By lncRNA profiling, novel lncRNAs related to NSCLC were identified. LNBC3 expression was quantified by qRT-PCR. Migration and viability assays were performed to evaluate the function of LNBC3 in vitro. In vivo xenograft model was conducted to determine the oncogenic functions of LNBC3. RNA immunoprecipitation (RIP) followed by mass spectrometry (MS) was utilized to identify BCL6 as LNBC3 binding target.
LNBC3 is markedly overexpressed in tumor tissues and NSCLC cell lines. Higher LNBC3 levels correlated with advanced TNM stages, larger tumor size, and metastasis. LNBC3 promoted NSCLC migration and viability. The in vivo experiments demonstrated that xenograft tumor growth and proliferation were facilitated with increasing LNBC3 levels. The antisense oligonucleotides (ASOs) targeting LNBC3 substantially inhibited lung cancer progression. Mechanistic studies showed that LNBC3 could interact with BCL6 leading to BCL6 stabilization through reduced proteasomal degradation.
Collectively, our data have identified a novel lncRNA LNBC3 in NSCLC progression. The LNBC3-BCL6 axis might be a potential target for pharmaceutical intervention.
非小细胞肺癌（NSCLC）是一种常见的恶性肿瘤，全球范围内都有大量报道表明长链非编码 RNA（lncRNA）在 NSCLC 中具有重要作用。然而，一种名为 LNBC3 的新型 lncRNA 的作用仍不清楚。
通过 lncRNA 谱分析，确定了与 NSCLC 相关的新型 lncRNA。通过 qRT-PCR 定量检测 LNBC3 的表达。通过迁移和活力测定来评估 LNBC3 在体外的功能。通过体内异种移植模型来确定 LNBC3 的致癌功能。采用 RNA 免疫沉淀（RIP）结合质谱（MS）技术鉴定 BCL6 是 LNBC3 的结合靶标。
在肿瘤组织和 NSCLC 细胞系中，LNBC3 明显过表达。较高的 LNBC3 水平与较晚的 TNM 分期、更大的肿瘤大小和转移相关。LNBC3 促进 NSCLC 的迁移和活力。体内实验表明，随着 LNBC3 水平的升高，异种移植肿瘤的生长和增殖得到促进。针对 LNBC3 的反义寡核苷酸（ASO）可显著抑制肺癌进展。机制研究表明，LNBC3 可与 BCL6 相互作用，通过减少蛋白酶体降解来稳定 BCL6。
综上所述，我们的数据在 NSCLC 进展中鉴定了一种新型 lncRNA LNBC3。LNBC3-BCL6 轴可能是药物干预的潜在靶点。
