Abstract
Hepatocellular carcinoma (HCC) is a significant cause of cancer-related mortality owing to resistance to traditional treatments and tumor recurrence after therapy, which leads to poor therapeutic outcomes. Cancer stem cells (CSC) are a small subset of tumor cells with the capability to influence self-renewal, differentiation, and tumorigenesis. A number of surface markers for liver cancer stem cell (LCSC) subpopulations (EpCAM, CD133, CD44, CD13, CD90, OV-6, CD47, and side populations) in HCC have been identified. LCSCs play critical roles in regulating HCC stemness, self-renewal, tumorigenicity, metastasis, recurrence, and therapeutic resistance via genetic mutations, epigenetic disruption, signaling pathway dysregulation, or alterations microenvironment. Accumulating studies have shown that biomarkers for LCSCs contribute to diagnosis and prognosis prediction of HCC, supporting their utility in clinical management and development of therapeutic strategies. Preclinical and clinical analyses of therapeutic approaches for HCC using small molecule inhibitors, oncolytic measles viruses, and anti-surface marker antibodies have demonstrated selective, efficient, and safe targeting of LCSC populations. The current review focuses on recent reports on the influence of LCSCs on HCC stemness, tumorigenesis, and multiple drug resistance (MDR), along with LCSC-targeted therapeutic strategies for HCC.
Highlights
Embryogenesis of both normal and tumor cells involves similar processes, including proliferation, motility, homing, dynamic morphologic changes, cellular heterogeneity, and interactions with the microenvironment
The current review focuses on recent reports on the influence of liver cancer stem cell (LCSC) on hepatocellular carcinoma (HCC) stemness, tumorigenesis, and multiple drug resistance (MDR), along with
CD133 expression in HCC tissues derived from patients with early recurrence. These results clearly suggest that VEGF and CD133+ stemness markers are positively correlated with early HCC
Summary
Embryogenesis of both normal and tumor cells involves similar processes, including proliferation, motility, homing, dynamic morphologic changes, cellular heterogeneity, and interactions with the microenvironment. Carcinogenesis is described as deregulation of malignant organogenesis regulated by abnormally proliferating and metastatic cancer and activated stromal cells that trigger angiogenesis, fibrosis, and inflammation [1] One such case is liver cancer, which is classified as primary or secondary. The above factors are correlated with multiple dysregulated signaling pathways, such as growth factor-mediated angiogenic signaling (vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin-like growth factor (IGF), hepatocyte growth factor (HGF)/c-MET), mitogen-activated protein kinase (MAPK), phosphatidylinositol-3 kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR), and Wnt/β-catenin pathways, which contribute to HCC development and tumorigenesis [8]. The functions of LCSCs in HCC and targeted therapeutic strategies are comprehensively discussed
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