Kai Zhu

The proliferation of hepatic progenitor cells (HPCs) is observed in reactive conditions of the liver and primary liver cancers. Ring1 as a member of polycomb‐group proteins which play vital roles in carcinogenesis and stem cell self‐renewal was increased in HCC patients and promoted proliferation and survival of cancer cell by degrading p53. However, the mechanisms of Ring1 driving the progression of hepatocarcinogenesis have not been elucidated. In this study, forced expression Ring1 and Ring1 siRNA lentiviral vectors were utilized to stably overexpression and silence Ring1 in HPC cell line (WB‐F344), respectively. Our finding indicated that overexpression of Ring1 in HPCs promoted colony formation, cell multiplication, and invasion in vitro, conversely depletion of Ring1 repressed the biological functions of HPCs relative to controls. The expression of β‐catenin was upregulated in the HPCs with overexpression of Ring1, and the correlation analysis also showed that β‐catenin and Ring1 had a significant correlation in the liver cancer tissues and adjacent tissues. The activation of the Wnt/β‐catenin signaling pathway significantly increased the expression of liver cancer stem cells related (LCSCs)‐related molecular markers CD90 and EpCAM, which led to the transformation of HPCs into LCSCs. Most importantly, the injection of HPCs with overexpressed Ring1 into the subcutaneous of nude mice leads to the formation of poorly differentiated HCC neoplasm. Our findings elucidate that overexpression of Ring1 the activated Wnt/β‐catenin signaling pathway and drove the transformation of HPCs into cancer stem cell‐like cells, suggesting Ring1 has extraordinary potential in early diagnosis of HCC.

Background: Our previous study showed that SUMO1 expression is closely related to progression in non‐small cell lung cancer (NSCLC); however, the function of SUMO1 in NSCLC has not yet been well elucidated.Methods: SUMO1 was enhanced or silenced in two NSCLC cell lines by using either forced SUMO1 expression or short hairpin RNA against SUMO1 lentiviral vectors, respectively. The biological functions of SUMO1 in NSCLC were investigated through colony‐formation, cell proliferation, and invasion assays, and cell cycle analysis. NF‐κB expression was detected in the overexpressed and silenced SUMO1 cell lines. Immunohistochemistry was used to detect an association between SUMO1 and NF‐κB in the cancer and adjacent tissues of 168 patients with lung cancer.Results: Overexpressed SUMO1 promoted the proliferation rate, colony formation ability, invasion, and NF‐κB expression in an A549 cell line. Conversely, SUMO1 depletion inhibited the cell growth rate, colony formation ability, invasion, and NF‐κB expression in a Calu‐1 cell line. SUMO1 expression was significantly correlated with NF‐κB expression in lung adenocarcinoma and squamous carcinoma patients (r > 0.5, P < 0.001).Conclusion: Our results provide evidence that SUMO1 promotes the proliferation and invasion of NSCLC cells by regulating NF‐κB.