journal contribution
posted on 2023-03-31, 01:24 authored by Zhen Cai, Zhen-Yu Qian, Hao Jiang, Ning Ma, Zhi Li, Li-Yu Liu, Xin-Xin Ren, Yu-Rong Shang, Jing-Jing Wang, Jing-Jing Li, Dong-Ping Liu, Xiu-Ping Zhang, Dan Feng, Qian-Zhi Ni, Yuan-Yuan Feng, Nan Li, Xiao-Yan Zhou, Xiang Wang, Ying Bao, Xue-Li Zhang, Yue-Zhen Deng, Dong Xie The supplementary infomation containing Figure legends, five supplemental figures and 3 supplemental tables. Figure S1 The higher expression of hPCL3s correlated with the poor survival of HCC patients. Figure S2 hPCL3s did not promote the tumorigenesis in vivo. Figure S3 The effects of hPCL3s on the growth of Hep3B, Huh7 and PVTT cells in a 48-hour time window were evaluated using MTT assay. Figure S4 Screening the signal pathways affected by hPCL3s. Figure S5 The AAV delivered Flag-hPCL3s was dominantly expressed in the liver. Table S1 Primer sequences. Table S2 The correlation between the expression of hPCL3s and clinical feature (Tissue array 2). Table S3 Microarray data.
Funding
National Natural Science Foundation of China
Youth Innovation Promotion Association, Chinese Academy of Sciences
CAS/SAFEA International Partnership Program for Creative Research Teams
Chinese Academy of Sciences, and Innovation-driven Program of the Central South University
History
ARTICLE ABSTRACT
Two isoforms of human Polycomb-like protein 3 (hPCL3) have been reported as components of the nuclear Polycomb repressive complex 2 (PRC2), with the short isoform (hPCL3s) showing a dominant cytoplasmic localization. The function of cytoplasmic hPCL3s has, however, not been addressed. In this study, we report that hPCL3s is upregulated in clinical hepatocellular carcinoma (HCC) samples and its expression correlated with HCC clinical features. hPCL3s positively regulated the migration, invasion, and metastasis of HCC cells. hPCL3s interacted with components of the cytoplasmic β-catenin destruction complex, inhibited β-catenin degradation, and activated β-catenin/T-cell factor signaling. Downstream of the β-catenin cascade, IL6 mediated the motility-promoting functions of hPCL3s. Forced expression of hPCL3s in the liver of a HCC mouse model promoted tumorigenesis and metastasis. Taken together, these data show that hPCL3s promotes the metastasis of HCC by activating the β-catenin/IL6 pathway.Significance: hPCL3s has an oncogenic role in hepatocellular carcinoma by activating the β-catenin/IL6 signaling axis to promote metastasis. Cancer Res; 78(10); 2536–49. ©2018 AACR.
