Department of Cardio-Thoracic Surgery, Wujin Hospital Affiliated with Jiangsu University (The Wujin Clinical College of Xuzhou Medical University), Changzhou City, Jiangsu Provence,213017, China.
Department of Oncology, Wujin Hospital Affiliated with Jiangsu University (The Wujin Clinical College of Xuzhou Medical University), Changzhou City, Jiangsu Provence, 213017, China.
Curr Pharm Biotechnol. 2023;24(8):1059-1069. doi: 10.2174/1389201023666220728143410.
LncRNA NBR2 is a key regulator in cancer metabolism. However, its role in lung cancer is unknown.
This study aimed to explore the function of NBR2 in non-small cell lung cancer (NSCLC), which is the most common type of lung cancer.
Paired NSCLC and non-cancer tissues were collected from 68 patients with NSCLC. The expression of NBR2 and transforming growth factor-β1 (TGF-β1) in these samples was analyzed by RT-qPCR. The prognostic value of NBR2 for NSCLC was explored by performing a 5-year follow-up study. The interaction between NBR2 and TGF-β1 in two NSCLC cell lines was detected by overexpression assay, followed by RT-qPCR and Western blot analysis. Flow cytometry was performed to evaluate the role of NBR2 and TGF-β1 in regulating NSCLC cell stemness.
NBR2 was significantly downregulated in NSCLC tissues than that in non-cancer tissues of NSCLC patients, and low expression levels of NBR2 predicted poor survival. TGF-β1 was significantly upregulated in NSCLC tissues than that in non-cancer tissues, and was inversely correlated with NBR2. Overexpression of NBR2 downregulated TGF-β1, while overexpression of TGF-β1 did not affect the expression of NBR2. Overexpression of NBR2 inhibited, while overexpression of TGF-β1 promoted NSCLC cell stemness. Overexpression of TGF-β1 attenuated the effects of overexpression of NBR2. Mechanically, NBR2 interacted with Notch1 protein to inhibit its expression, thereby inhibiting the expression of TGF-β1 and further affecting the proportion of CD133+ cells.
LncRNA NBR2 regulates cancer cell stemness and predicts survival in NSCLC possibly by downregulating TGF-β1 through Notch1.
LncRNA NBR2 是癌症代谢中的关键调节因子。然而，其在肺癌中的作用尚不清楚。
本研究旨在探讨 NBR2 在非小细胞肺癌（NSCLC）中的功能，这是非小细胞肺癌中最常见的类型。
收集 68 例 NSCLC 患者的配对 NSCLC 组织和非癌组织。通过 RT-qPCR 分析这些样本中 NBR2 和转化生长因子-β1（TGF-β1）的表达。通过进行 5 年随访研究探讨 NBR2 对 NSCLC 的预后价值。通过过表达实验检测两种 NSCLC 细胞系中 NBR2 和 TGF-β1 之间的相互作用，然后进行 RT-qPCR 和 Western blot 分析。通过流式细胞术评估 NBR2 和 TGF-β1 在调节 NSCLC 细胞干性中的作用。
NBR2 在 NSCLC 组织中的表达明显低于 NSCLC 患者非癌组织，低表达水平预示着不良预后。TGF-β1 在 NSCLC 组织中的表达明显高于非癌组织，与 NBR2 呈负相关。NBR2 的过表达下调 TGF-β1，而过表达 TGF-β1 不影响 NBR2 的表达。NBR2 的过表达抑制，而过表达 TGF-β1 促进 NSCLC 细胞干性。TGF-β1 的过表达减弱了 NBR2 过表达的作用。机制上，NBR2 与 Notch1 蛋白相互作用抑制其表达，从而抑制 TGF-β1 的表达，进一步影响 CD133+细胞的比例。
LncRNA NBR2 通过 Notch1 下调 TGF-β1 来调节癌细胞干性并预测 NSCLC 的生存，可能。
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