Cui Guangying, Wang Huifen, Liu Wenli, Xing Jiyuan, Song Wengang, Zeng Zhaohai, Liu Liwen, Wang Haiyu, Wang Xuemei, Luo Hong, Leng Xiaoyang, Shen Shen
Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Gene Hospital of Henan Province, Precision Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Front Cell Dev Biol. 2020 Nov 25;8:566494. doi: 10.3389/fcell.2020.566494. eCollection 2020.
Glycogen metabolism plays a key role in tumorigenesis. High expression levels of glycogen phosphorylase B (PYGB) were reported in several cancers and might be served as a prognostic biomarker for cancer from precancerous lesions. Previous studies indicated the high expression of PYGB in hepatocellular carcinoma (HCC) tissues. However, the detailed roles of PYGB in HCC, as well as the regulatory mechanisms, are still unclear. In this study, we confirmed that PYGB was overexpressed in HCC tissues. PYGB overexpression was significantly associated with an aggressive tumor phenotype and poor prognosis of HCC patients. Functionally, PYGB knockdown suppressed HCC cell proliferation, migration and invasion , as well as tumorigenesis and metastasis . Bioinformatics analysis indicated that PYGB overexpression might enhance epithelial to mesenchymal transition (EMT) in HCC. Moreover, miR-101-3p was identified to post-transcriptionally inhibit the expression of PYGB via binding to 3'-UTR of PYGB. Overexpression of PYGB antagonized the regulatory effect of miR-101-3p on cell proliferation, migration and invasion in HCC cells. In summary, our results suggest that miR-101-3p/PYGB axis has an important role in HCC and PYGB could be served as a novel prognostic biomarker and therapeutic target for improving the prognosis of HCC patients.
糖原代谢在肿瘤发生过程中起着关键作用。据报道,糖原磷酸化酶B(PYGB)在多种癌症中高表达,可能作为癌前病变向癌症发展的预后生物标志物。先前的研究表明PYGB在肝细胞癌(HCC)组织中高表达。然而,PYGB在HCC中的具体作用以及调控机制仍不清楚。在本研究中,我们证实PYGB在HCC组织中过表达。PYGB过表达与HCC患者侵袭性肿瘤表型和不良预后显著相关。在功能上,敲低PYGB可抑制HCC细胞增殖、迁移和侵袭,以及肿瘤发生和转移。生物信息学分析表明,PYGB过表达可能增强HCC中的上皮-间质转化(EMT)。此外,已确定miR-101-3p通过与PYGB的3'-UTR结合在转录后抑制PYGB的表达。PYGB的过表达拮抗了miR-101-3p对HCC细胞增殖、迁移和侵袭的调控作用。总之,我们的结果表明miR-101-3p/PYGB轴在HCC中起重要作用,并且PYGB可作为改善HCC患者预后的新型预后生物标志物和治疗靶点。