hDlk-1: a cell surface marker common to normal hepatic stem/progenitor cells and carcinomas.
ABSTRACT Advances in stem cell biology have clarified that a tumour is a collection of heterogeneous cell populations, and that only a small fraction of tumour cells possesses the potential to self-renew. Delta-like 1 protein (Dlk-1) is a surface antigen present on foetal hepatic stem/progenitor cells but absent from mature hepatocytes in neonatal and adult rodent liver. Using a monoclonal antibody (mAb) against hDlk-1, Yanai et al. (Dlk-1, a cell surface antigen on foetal hepatic stem/progenitor cells, is expressed in hepatocellular, colon, pancreas and breast carcinomas at a high frequency. J. Biochem. 2010;148:85-92) have shown that human (h) Dlk-1 is expressed in human foetal, but not adult, liver and that 20% of all hepatocellular carcinomas (HCCs) are hDlk-1(+). Importantly, an even higher percentage of HCCs in younger patients are hDLK-1(+). These authors also found that hDlk-1 is present at high frequency in colon adenocarcinomas, pancreatic islet carcinomas and small cell lung carcinomas. Here, I discuss the implications of the expression of foetal hepatic stem/progenitor cell antigens on carcinoma cells.
- SourceAvailable from: onlinelibrary.wiley.com[Show abstract] [Hide abstract]
ABSTRACT: Liver stem/progenitor cells (LSPCs) are able to duplicate themselves and differentiate into each type of cells in the liver, including mature hepatocytes and cholangiocytes. Understanding how to accurately control the hepatic differentiation of LSPCs is a challenge in many fields from preclinical to clinical treatments. This review summarizes the recent advances made to control the hepatic differentiation of LSPCs over the last few decades. The hepatic differentiation of LSPCs is a gradual process consisting of three main steps: initiation, progression and accomplishment. The unbalanced distribution of the affecting materials in each step results in the hepatic maturation of LSPCs. As the innovative and creative works for generating hepatocytes with full functions from LSPCs are gradually accumulated, LSPC therapies will soon be a new choice for treating liver diseases.Journal of Cellular and Molecular Medicine 11/2013; · 3.70 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Cell therapy may be a novel and effective treatment strategy for liver diseases, replacing liver transplantation. The potential of two alternative cell types (hepatic progenitor/stem cells and mature hepatocytes) has not yet been fully assessed; the issues of low amplification efficiency and recovery function remain to be resolved. In this study, we investigated the proliferation, differentiation and function of primary mouse mature hepatocytes and embryonic hepatic progenitor cells. Primary cells were obtained from the livers of mouse embryos at 14.5 days post coitus [hepatic progenitor 14.5d (HP14.5d) cells], as well as from the livers of 3-month-old mice [liver cells 3m (LC3m)]. Using trypan blue staining and crystal violet staining to detect cell viability, we found that compared with the limited growth capability of primary LC3m cells, primary HP14.5d cells exhibited an active cell proliferation; however, proliferative ability of passaged HP14.5d cells significantly decreased. After the HP14.5d cells were treated in hepatic induction medium, the expression of progenitor cell markers decreased and that of mature hepatic markers increased, to levels similar to those of LC3m cells. On day 12 of induction, the HP14.5d cells showed comparable indocyanine green (ICG) uptake and glycogen storage to that of the LC3m cells. Therefore, our study demonstrates that primary hepatic progenitor cells have a stronger proliferation capacity and differentiation potential, supporting their clinical application in liver cell transplantation.International Journal of Molecular Medicine 06/2013; · 1.88 Impact Factor