lncRNA FEZF1-AS1 通过 P53 信号通路在结直肠癌进展中的作用

Minglu Ding, Wanyao Wang, Keyuan Huo, Yidan Song, Xiaojie Chen, Zihan Xiang, Peijian Chen, Lantao Liu
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引用次数: 0

摘要

长非编码 RNA(lncRNA)已成为结直肠癌(CRC)发病过程中的关键调控因子。先前的研究表明,lncRNA FEZF1-AS1 在 CRC 中高表达,但其通过 P53 信号通路调节 CRC 的作用仍不清楚。本研究发现,FEZF1-AS1能促进CRC细胞系(HCT116)的生长,并通过P53信号通路驱动上皮-间质转化(EMT)。我们的数据显示,FEZF1-AS1在HCT116中表达明显上调,而FEZF1-AS1水平的升高与CRC患者的不良预后有关。此外,敲除 FEZF1-AS1 还能通过诱导细胞周期停滞明显抑制 HCT116 的增殖。敲除FEZF1-AS1还能通过抑制P53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。综上所述,本研究证实了FEZF1-AS1通过P53信号通路和抑制EMT调控结HCT116的生长,为CRC的潜在治疗策略提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Role of lncRNA FEZF1-AS1 in Colorectal Cancer Progression Via the P53 Signaling Pathway.

Long noncoding RNAs (lncRNAs) have emerged as critical regulators in the development of colorectal cancer (CRC). Previous studies indicate that lncRNA FEZF1-AS1 is highly expressed in CRC, but its role in modulating CRC via the P53 signaling pathway remains unclear. In this study, we found that FEZF1-AS1 promotes the growth of the CRC cell line (HCT116) and drives epithelial-mesenchymal transition (EMT) through the P53 signaling pathway. Our data showed that FEZF1-AS1 expression is significantly upregulated in HCT116, and elevated levels of FEZF1-AS1 are associated with poor prognosis in patients with CRC. In addition, the knockdown of FEZF1-AS1 markedly inhibited the proliferation of HCT116 by inducing cell cycle arrest. Knockdown of FEZF1-AS1 depletion also led to apoptosis in CRC cells by suppressing the P53 signaling pathway and EMT, thereby reducing their viability, proliferation, migration, and invasion. In summary, this study confirmed that FEZF1-AS1 regulates the growth of junction HCT116 through P53 signaling pathway and inhibiting EMT, providing new insights for the potential therapeutic strategies against CRC.

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