Journal of Stem Cell Research & Therapy

Origins of Cancer Stem Cells and their Relevance to Cancer

Hailey Careter^* Department of Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
^*Correspondence: Hailey Careter, Department of Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA, Email:

Received: 12-Jan-2023, Manuscript No. JSCRT-23-20718; Editor assigned: 16-Jan-2023, Pre QC No. JSCRT-23-20718(PQ); Reviewed: 06-Feb-2023, QC No. JSCRT-23-20718; Revised: 16-Feb-2023, Manuscript No. JSCRT-23-20718(R); Published: 24-Feb-2023, DOI: 10.35248/2157-7633.23.13.577

Description

Cancer is a complex and multifactorial disease, with a wide variety of cell types and genetic alterations that contribute to its development and progression. The concept of Cancer Stem Cells (CSCs) has gained significant attention in recent years, as it provides a potential explanation for the heterogeneity of cancer cells within a tumor and their resistance to treatment. CSCs are a small population of cells within a tumor that possess stem celllike properties, such as self-renewal and differentiation, and are thought to be responsible for tumor initiation, maintenance, and metastasis. In this article, we will explore the current understanding of CSCs, their properties, and their potential implications for cancer treatment. CSCs are characterized by their ability to self-renew and differentiate into various cell types that make up the tumor [1-5]. They are also capable of initiating tumors when transplanted into immune compromised mice, demonstrating their tumorigenic potential. CSCs share many properties with normal stem cells, including the expression of stem cell markers such as CD44, CD133, and ALDH1, and the ability to form spheroids in vitro. One of the key features of CSCs is their resistance to conventional cancer therapies, such as chemotherapy and radiation. This is thought to be due to their ability to enter a quiescent state, or a slow cycling state, which renders them less susceptible to these treatments. Additionally, CSCs have been shown to possess enhanced DNA repair mechanisms and anti-apoptotic pathways, which further contribute to their resistance. CSCs also play a role in tumor metastasis, the spread of cancer cells from the primary tumor to other parts of the body. CSCs have been shown to be involved in the process of Epithelial-To-Mesenchymal Transition (EMT), a process by which cells lose their epithelial characteristics and acquire mesenchymal traits, allowing them to become more mobile and invasive. CSCs that undergo EMT are thought to be responsible for the formation of metastases in distant organs.

The origin of CSCs is still a topic of debate. There are two main hypotheses: the stochastic model and the hierarchical model. The stochastic model proposes that all cancer cells have the potential to become CSCs through random genetic mutations or epigenetic changes. In contrast, the hierarchical model proposes that CSCs arise from a distinct subset of cells with stem cell-like properties. Evidence supporting the hierarchical model comes from studies that have identified specific cell populations within tumors that possess stem cell-like properties and are responsible for tumor initiation and maintenance [6-9]. These cells are often found at the tumor periphery, where they interact with the tumor microenvironment and receive signals that promote their self-renewal and survival. However, recent studies have challenged the hierarchical model by demonstrating that CSCs can arise from non-stem cells through reprogramming. This process involves the activation of stem cell-like gene expression programs in non-stem cells, which confers them with stem celllike properties and allows them to become CSCs. The existence of CSCs has significant implications for cancer treatment. Conventional cancer therapies, such as chemotherapy and radiation, target rapidly dividing cells and are less effective against quiescent cells, such as CSCs. Therefore, therapies that specifically target CSCs may be more effective in eliminating tumors and preventing relapse. One approach to targeting CSCs is through the use of drugs that interfere with self-renewal pathways. These drugs inhibit the signaling pathways that promote self-renewal and induce CSC differentiation, leading to the depletion of the CSC population [10,11].

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