Zhang Haiping, Chu Kaiqiu, Zheng Chunxi, Ren Lisheng, Tian Runhua
Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.
Department of Clinical Laboratory, Qingdao Women and Children's Hospital, Qingdao, China.
Front Genet. 2020 Jul 22;11:666. doi: 10.3389/fgene.2020.00666. eCollection 2020.
Hepatocellular Carcinoma (HCC) currently remains one of the most lethal malignancies worldwide. Recently, long non-coding RNAs (lncRNAs) had been demonstrated to play a crucial role in the progression of multiple human cancers, including HCC. In this study, we found that lncRNA DUXAP8 was upregulated in tumor samples and served as an oncogene in HCC. Bioinformatics analysis showed that DUXAP8 was significantly associated with the regulation of centrosome organization, homologous recombination, meiotic cell cycle process, sister chromatid segregation, nuclear chromosome segregation, and RNA export from the nucleus. The knockdown of DUXAP8 significantly suppresses cell proliferation and the cell cycle but induces cell apoptosis in HCC. Mechanically, the present study showed that DUXAP8 serves as a sponge of MiR-490-5p to promote the expression of BUB1 in HCC. Although the underlying regulatory mechanisms of DUXAP8 in HCC require further investigation, this study, for the first time, showed that DUXAP8 can serve as a new therapeutic target for HCC.
肝细胞癌(HCC)目前仍然是全球最致命的恶性肿瘤之一。最近,长链非编码RNA(lncRNAs)已被证明在包括HCC在内的多种人类癌症进展中发挥关键作用。在本研究中,我们发现lncRNA DUXAP8在肿瘤样本中上调,并在HCC中作为癌基因发挥作用。生物信息学分析表明,DUXAP8与中心体组织调控、同源重组、减数分裂细胞周期进程、姐妹染色单体分离、核染色体分离以及RNA从细胞核输出显著相关。敲低DUXAP8可显著抑制HCC细胞增殖和细胞周期,但诱导细胞凋亡。机制上,本研究表明DUXAP8作为MiR-490-5p的海绵,促进HCC中BUB1的表达。尽管DUXAP8在HCC中的潜在调控机制需要进一步研究,但本研究首次表明DUXAP8可作为HCC的新治疗靶点。