SPARC promotes epithelial-mesenchymal transition of hepatocellular carcinoma cells and acquisition of cancer stem cell phenotypes



SPARC is a matricellular glycoprotein plays a significant role in tumor development. SPARC has been indicated that promotes tumorigenesis, metastasis and poor prognosis in prostate cancer and lung cancer. Therefore, we sought to investigate the molecular mechanisms of SPARC in regulating hepatocellular carcinoma (HCC).


We used spheroids cultured in serum-free culture medium (SFM) to obtain liver cancer stem cells. Flow cytometric analysis were performed to investigate percentage of CD133+cells in liver cancer cells. Real-time polymerase chain reaction (PCR) and western blot were used to assess gene expression in cell lines. Transwell and Wound healing assays were performed to indicated cell migration of HCC.


SPARC was upregulated in spheres formation in HCC cells. Overexpression of SPARC enhanced the ability to form tumor spheres and increased CD133 and Oct4 expression. Besides, SPARC promoted the migration and epithelial-mesenchymal transition (EMT) in HCC cells. Importantly, SPARC overexpression stimulated the formation of subcutaneous tumors in nude mice.


Our findings suggest that SPARC overexpression promotes tumor growth, inducing EMT and acquisition of a stem cell phenotype. What’s more, research elucidating the biological mechanisms of SPARC may be beneficial to liver cancer treatment.