Liver cancer stem cell markers and signaling pathways (LCSC markers/signaling)

Liver cancer stem cells (LCSCs) represent a distinct subpopulation of cells within liver tumors, such as hepatocellular carcinoma (HCC), that exhibit stem-like properties including self-renewal and the ability to generate heterogeneous lineages of cancer cells [NIH, 2019]. These cells are identified by a variety of surface markers, most notably CD133 (Prominin-1), CD44, EpCAM, and CD90, which often correlate with poor clinical prognosis and high rates of recurrence [MDPI, 2021]. The maintenance and expansion of LCSCs are regulated by several key developmental signaling pathways, including Wnt/beta-catenin, Notch, Hedgehog, and TGF-beta, which are frequently dysregulated in liver cancer [NIH, 2015]. Because LCSCs are highly resistant to standard chemotherapy and radiation, they are considered a major driver of treatment failure and metastatic spread [PubMed, 2019]. Therapeutic efforts are currently focused on developing agents that can specifically target LCSC markers or inhibit their essential signaling pathways to eliminate this resilient cell population [NIH, 2019]. However, the clinical application of these therapies is complicated by the potential for toxicity to normal stem cells and the complex crosstalk between different signaling networks [NIH, 2015].

Other names

Hepatic cancer stem cell markersLiver tumor-initiating cell markersLCSC signalingLiver CSC markers

Inhibition of self-renewal signaling pathways (Wnt, Notch, Hedgehog, STAT3), blockade of LCSC-specific surface markers (CD133, CD44, EpCAM), and induction of differentiation or apoptosis in the stem-like subpopulation [NIH, 2015; OAepublish, 2019].