Abstract
Cancer stem cells (CSCs) and epithelial‑mesenchymal transition (EMT) are critical factors contributing to tumor metastasis and recurrence. The BMI1 proto‑oncogene (Bmi‑1) promotes the development and progression of hematologic malignancies and of several types of solid tumors. The aim of the present study was to explore the mechanism by which Bmi‑1 may promote invasion and migration of hepatocellular carcinoma Hep G2 cells. CD133 antigen is a transmembrane glycoprotein and regarded as a cancer stem cells marker in hepatocellular carcinoma. CD133+Hep G2 cells were enriched by magnetic‑activated cell sorting and exhibited greater viability compared with CD133‑Hep G2 cells, as measured by Cell Counting kit‑8 assay. Then, Bmi‑1 was overexpressed in CD133+Hep G2 cells by transfection with the Bmi‑1/pcDNA3.1(+) expression plasmid, and overexpression was confirmed by reverse‑transcription‑polymerase chain reaction and western blotting. Overexpression of Bmi‑1in CD133+Hep G2 cells resulted in the downregulation of E‑cadherin and upregulation of Vimentin at the protein level. The invasion and migration abilities of CD133+Hep G2 cells were increased in the Bmi‑1/pcDNA3.1(+)‑transfected group, as measured by Transwell invasion and wound healing assays, respectively. In conclusion, Bmi‑1 promoted invasion and migration of CD133+Hep G2 cells most likely through inducing EMT. The present findings may offer a potential novel target for the development of hepatocellular carcinoma therapies.
Highlights
The Polycomb group (PcG) of proteins consists of transcriptional repressors that orchestrate changes in chromatin structure to regulate gene activity [1,2]
The results demonstrated that CD133+hepatocellular carcinoma G2 (Hep G2) cells exhibited increased migration (Fig. 4) and invasion (Fig. 5) abilities following Bmi‐1 overexpression, compared with control cells
These findings indicate that Bmi‐1 promoted invasion and migration of CD133+Hep G2 cells, and this effect may be associated with inducing Epithelial‐mesenchymal transition (EMT)
Summary
The Polycomb group (PcG) of proteins consists of transcriptional repressors that orchestrate changes in chromatin structure to regulate gene activity [1,2]. The BMI1 proto‐oncogene (Bmi‐1), a member of PcG proteins, was previously known as a transcriptional repressor targeting the cyclin‐dependent kinase inhibitor 2A gene locus. Bmi‐1 is described as an oncogene in many tumor types and has critical roles in the oncogenesis of cancers and cancer stem cells (CSCs) [3]. The discovery of CSC‐specific markers has helped identify CSC population in many cancer types, including blood, neck, thoracic, abdominal and genital system cancers [7,8,9,10,11,12,13,14,15]. The downregulation or loss of E‐cadherin and the upregulation of Vimentin are regarded as hallmarks of EMT [18]
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