Chen Yu-Hsuan, Yang Chih-Yun, Liu Pei-Jung, Hu Wan-Chung, Lu Kuo-Cheng, Cheng Ching-Feng, Tsai Kuo-Wang
Division of Chest Medicine, Department of Internal Medicine, CHENG HSIN General Hospital, Taipei, Taiwan, R.O.C.
Division of Chest Medicine, Kaohsiung Municipal Min-Sheng Hospital, Kaohsiung, Taiwan, R.O.C.
Cancer Genomics Proteomics. 2025 Sep-Oct;22(5):775-790. doi: 10.21873/cgp.20536.
BACKGROUND/AIM: Lung cancer is the most prevalent type of cancer and the leading cause of cancer-related mortality worldwide. Understanding the detailed mechanisms of lung carcinogenesis can improve the survival rates of patients with lung cancer. Long noncoding RNAs (lncRNAs) are large (>200 nucleotides) noncoding RNAs that play a key role in various types of human cancer by regulating the proliferation, apoptosis, and metastasis of cancer cells. LOC100506691 is an oncogene that promotes the growth and metastasis of cancer cells. However, its biological role in lung cancer remains unknown. MATERIALS AND METHODS: The expression levels and clinical significance of LOC100506691 in lung cancer were analyzed using public databases. The biological function of LOC100506691 was investigated in lung cancer cell lines following siRNA-mediated knockdown, with assessments of cell proliferation, colony formation, motility, apoptosis, and cell cycle progression. Potential signaling pathways affected by LOC100506691 knockdown were examined through western blotting and pathway enrichment analysis. RESULTS: According to public databases, the expression of LOC100506691 is significantly higher in lung cancer cells than in adjacent normal tissues. These high expression levels of LOC100506691 are strongly associated with poor survival outcomes in patients with lung cancer. Knockdown of LOC100506691 significantly suppresses the proliferation, colony formation ability, and metastasis of lung cancer cells. In lung cancer cells, LOC100506691 knockdown impairs the cell cycle progression and induces apoptosis by modulating the PI3K/AKT signaling pathway. CONCLUSION: Our findings indicate that LOC100506691 is a novel lncRNA that promotes the growth and metastasis of lung cancer cells and therefore provide valuable insights that can aid in the development of lung cancer therapy.
背景/目的:肺癌是全球最常见的癌症类型,也是癌症相关死亡的主要原因。了解肺癌发生的详细机制可提高肺癌患者的生存率。长链非编码RNA(lncRNAs)是长度大于200个核苷酸的非编码RNA,通过调节癌细胞的增殖、凋亡和转移,在各类人类癌症中发挥关键作用。LOC100506691是一种促进癌细胞生长和转移的癌基因。然而,其在肺癌中的生物学作用尚不清楚。 材料与方法:利用公共数据库分析LOC100506691在肺癌中的表达水平及临床意义。在肺癌细胞系中,通过小干扰RNA(siRNA)介导的敲低技术研究LOC100506691的生物学功能,并评估细胞增殖、集落形成、迁移、凋亡和细胞周期进程。通过蛋白质免疫印迹法和通路富集分析,检测受LOC100506691敲低影响的潜在信号通路。 结果:根据公共数据库,LOC100506691在肺癌细胞中的表达明显高于相邻正常组织。LOC100506691的这些高表达水平与肺癌患者的不良生存结果密切相关。敲低LOC100506691可显著抑制肺癌细胞的增殖、集落形成能力和转移。在肺癌细胞中,敲低LOC100506691会损害细胞周期进程,并通过调节PI3K/AKT信号通路诱导凋亡。 结论:我们的研究结果表明,LOC100506691是一种新型lncRNA,可促进肺癌细胞的生长和转移,因此为肺癌治疗的发展提供了有价值的见解。
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