BCL6公司
癌症研究
肝细胞癌
细胞生长
细胞
生物
小RNA
细胞培养
基因敲除
基因沉默
下调和上调
细胞周期
癌基因
长非编码RNA
癌变
分子生物学
免疫学
B细胞
基因
抗体
生发中心
生物化学
遗传学
作者
Huaiyu Ding,Juan He,Weili Xiao,Zhihong Ren,Wanting Gao
出处
期刊:Research Square - Research Square
日期:2020-09-24
被引量:2
标识
DOI:10.21203/rs.3.rs-79374/v1
摘要
Abstract Background: PCED1B-AS1 has been characterized as an oncogene in glioma, while its role in hepatocellular carcinoma (HCC) is unknown. This study was performed to analyze the involvement of PCED1B-AS1. Methods: Expression of PCED1B-AS1 in paired HCC and non-tumor tissues from 62 HCC patients was determined by RT-qPCR. The correlation between PCED1B-AS1 and miR-10a or BCL6 was analyzed by linear regression. The 62 HCC patients were followed up for 5 years to analyze the prognostic value of PCED1B-AS1 for HCC. The interactions among PCED1B-AS1, miR-10a and BCL6 were analyzed by overexpression experiments. Cell proliferation was analyzed by CCK-8 assay. Results: PCED1B-AS1 was upregulated in HCC and predicted poor survival. Across HCC tissues, PCED1B-AS1 was inversely correlated with miR-10a, and positively correlated with BCL6 mRNA. In HCC cells, PCED1B-AS1 overexpression mediated the downregulation of miR-10a and upregulation of BCL6. Moreover, PCED1B-AS1 overexpression reduced the inhibitory effects of miR-10a overexpression on BCL6 expression and cell proliferation. Conclusions: PCED1B-AS1 is overexpressed in HCC and regulates miR-10a/BCL6 axis to promote cell proliferation.
科研通智能强力驱动
Strongly Powered by AbleSci AI