Ding Minglu, Wang Wanyao, Huo Keyuan, Song Yidan, Chen Xiaojie, Xiang Zihan, Chen Peijian, Liu Lantao
Mudanjiang Medical University, Mudanjiang, China.
School of Basic Medicine, Mudanjiang Medical University, Mudanjiang, China.
DNA Cell Biol. 2025 Jan;44(1):32-45. doi: 10.1089/dna.2024.0184. Epub 2024 Nov 6.
Long noncoding RNAs (lncRNAs) have emerged as critical regulators in the development of colorectal cancer (CRC). Previous studies indicate that lncRNA is highly expressed in CRC, but its role in modulating CRC via the signaling pathway remains unclear. In this study, we found that promotes the growth of the CRC cell line (HCT116) and drives epithelial-mesenchymal transition (EMT) through the signaling pathway. Our data showed that expression is significantly upregulated in HCT116, and elevated levels of are associated with poor prognosis in patients with CRC. In addition, the knockdown of markedly inhibited the proliferation of HCT116 by inducing cell cycle arrest. Knockdown of depletion also led to apoptosis in CRC cells by suppressing the signaling pathway and EMT, thereby reducing their viability, proliferation, migration, and invasion. In summary, this study confirmed that regulates the growth of junction HCT116 through signaling pathway and inhibiting EMT, providing new insights for the potential therapeutic strategies against CRC.
长链非编码RNA(lncRNAs)已成为结直肠癌(CRC)发展过程中的关键调节因子。先前的研究表明,lncRNA在CRC中高表达,但其通过信号通路调节CRC的作用仍不清楚。在本研究中,我们发现通过信号通路促进CRC细胞系(HCT116)的生长并驱动上皮-间质转化(EMT)。我们的数据显示,在HCT116中表达显著上调,并且其水平升高与CRC患者的不良预后相关。此外,敲低通过诱导细胞周期停滞显著抑制HCT116的增殖。敲低耗尽还通过抑制信号通路和EMT导致CRC细胞凋亡,从而降低其活力、增殖、迁移和侵袭能力。总之,本研究证实通过信号通路和抑制EMT调节连接HCT116的生长,为针对CRC的潜在治疗策略提供了新的见解。