Document Type : Review Article
Authors
1
Department of Hematology, Mashhad University of Medical Sciences, Mashhad, Iran
2
Department of Laboratory Science, Faculty of medicine, Semnan University of Medical Sciences, Semnan, Iran.
3
Department of Laboratory Sciences, Sabzevar University of Medical Sciences, Sabzevar, Iran.
4
Department of Occupational Therapy, School of Health Professions, University of Missouri, Columbia, Missouri, USA.
5
Department of Laboratory Science, Faculty of medicine, Semnan University of Medical Sciences, Semnan, Iran.
Abstract
Cancer stem cells (CSCs) are a subset of cells within tumors that exhibit stem cell-
like characteristics, including the ability to self-renew and differentiate. CSCs are the
cause of carcinogenesis and tumorigenesis. The expression of cell surface markers,
which varies linked to the kind of tumor, is utilized to recognize CSCs. An essential
part of tumor invasion and metastasis is played by CSCs. Numerous investigations
have been carried out to find distinguished markers and different phenotypes of CSCs,
which are especially crucial for identifying and separating this subset of cells. It was
discovered that the regulation of CSCs involves a multitude of signaling pathways.
These cells are determined by their ability to self-renewal pathways such as Wnt/β-
catenin, JAK/STAT3, PTEN/PI3-K/Akt, and Hedgehog, their surface biomarkers,
and their resistance to many drugs. Aberrant activation of these signaling pathways is
associated with cell growth. Thus, focusing on CSCs is seen to be a viable anti-cancer
treatment approach. It is encouraging that CSCs' self-renewal pathways present a
viable target for changing their survival tactics and limiting their capacity to
proliferate tumors. This study highlights the characterization and investigation of
CSC self-renewal pathways, also discusses potential targeted therapy for CSC, and
gives a summary of the significant factors and pathways that adjust CSC formation.
Keywords: Cancer Stem cells, Self-renewal, Tumor recurrence, Molecular Signaling,
targeted therapy
Keywords