Yuan Yixiao, Jiang Xiulin, Tang Lin, Wang Juan, Zhang Dahang, Cho William C, Duan Lincan
The Department of Thoracic Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, China.
Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences/ Kunming Institute of Zoology, Kunming, China.
Front Mol Biosci. 2022 Feb 8;8:785767. doi: 10.3389/fmolb.2021.785767. eCollection 2021.
Lung cancer is the most common cancer with high mortality. Increasing evidence has demonstrated that nonstructural maintenance of chromosomes condensin I complex subunit G (NCAPG) plays a crucial role in the progression of human cancers. However, the biological function and underlying mechanism of NCAPG in non-small cell lung cancer (NSCLC) are still unclear. Here, we utilized diverse public databases to analyze the expression of NCAPG in pan-cancer. We found that NCAPG was highly expressed in various human cancers, especially in NSCLC. NCAPG expression was significantly positively correlated with poor clinical-pathological features, poor prognosis, tumor mutational burden, DNA microsatellite instability, and immune cell infiltration in NSCLC. In addition, our results showed that depletion of NCAPG significantly inhibited NSCLC cell proliferation, migration, and self-renewal abilities, yet these could be reversed by adding microRNA (miRNA)-214-3p. Knockdown of long noncoding RNA (lncRNA) thymidylate synthetase opposite strand (TYMSOS) also inhibits the NSCLC cell proliferation, migration, and self-renewal abilities. In summary, our findings demonstrated that the crucial roles of the FOXM1/lncRNA-TYMSOS/miRNA-214-3p/NCAPG axis in NSCLC may shed light on how NCAPG may act as a therapeutic target for NSCLC.
肺癌是最常见且死亡率高的癌症。越来越多的证据表明,染色体凝聚素I复合体亚基G的非结构维持(NCAPG)在人类癌症进展中起关键作用。然而,NCAPG在非小细胞肺癌(NSCLC)中的生物学功能及潜在机制仍不清楚。在此,我们利用多种公共数据库分析了NCAPG在泛癌中的表达。我们发现NCAPG在各种人类癌症中高表达,尤其是在NSCLC中。在NSCLC中,NCAPG表达与不良临床病理特征、不良预后、肿瘤突变负荷、DNA微卫星不稳定性及免疫细胞浸润显著正相关。此外,我们的结果表明,NCAPG的缺失显著抑制NSCLC细胞的增殖、迁移和自我更新能力,但通过添加微小RNA(miRNA)-214-3p可逆转这些作用。长链非编码RNA(lncRNA)胸苷酸合成酶反义链(TYMSOS)的敲低也抑制NSCLC细胞的增殖、迁移和自我更新能力。总之,我们的研究结果表明,FOXM1/lncRNA-TYMSOS/miRNA-214-3p/NCAPG轴在NSCLC中的关键作用可能为NCAPG如何成为NSCLC的治疗靶点提供线索。