Targeting Cancer Stem Cells as the Key Driver of Carcinogenesis and Therapeutic Resistance

Abstract

The emerging concept of cancer stem cells (CSCs) as the key driver behind carcinogenesis, progression, and diversity has displaced the prior model of a tumor composed of cells with similar subsequently acquired mutations and an equivalent capacity for renewal, invasion, and metastasis. This significant change has shifted the research focus toward targeting CSCs to eradicate cancer. CSCs may be characterized using cell surface markers. They are defined by their capacity to self-renew and differentiate, resist conventional therapies, and generate new tumors following repeated transplantation in xenografted mice. CSCs’ functional capabilities are governed by various intracellular and extracellular variables such as pluripotency-related transcription factors, internal signaling pathways, and external stimuli. Numerous natural compounds and synthetic chemicals have been investigated for their ability to disrupt these regulatory components and inhibit stemness and terminal differentiation in CSCs, hence achieving clinical implications. However, no cancer treatment focuses on the biological consequences of these drugs on CSCs, and their functions have been established. This article provides a biomedical discussion of cancer at the time along with an overview of CSCs and their origin, features, characterization, isolation techniques, signaling pathways, and novel targeted therapeutic approaches. Additionally, we highlighted the factors endorsed as controlling or helping to promote stemness in CSCs. Our objective was to encourage future studies on these prospective treatments to develop a framework for their application as single or combined therapeutics to eradicate various forms of cancer.

Global research landscape and trends of cancer stem cells from 1997 to 2023: A bibliometric analysis

“…[ 59 , 60 ] However, There are several drawbacks that limit the clinic applications in currently available anti-CSCs drugs and therapies, including limited solubility, low stability, high toxicity, and lack of tissue selectivity. [ 61 ] Hence, even the CSCs transformation research is not shown in our bibliometric analysis results, it is also need more attention and development.…”

Cyclin Dependent Kinase Inhibitor 2A Genetic and Epigenetic Alterations Interfere with Several Immune Components and Predict Poor Clinical Outcome

“…Carcinogenesis is a complex process that involves several components to drive the cell from its normal state into a cancerous one [ 47 ]. CDKN2A is a gene that belongs to the category of tumor suppressor genes and the malfunction of these genes participates in tumor initiation [ 2 ].…”

Oncogenic Potential of Replication Factor C Subunit 4: Correlations with Tumor Progression and Assessment of Potential Inhibitors

“…The oncogene overexpression in cancerous tissues is a distinguishing feature of malignancy [ 52 ]. Therefore, in the initial stage of this study, we employed data from the Tumor Immune Estimation Resource, version 2 (TIMER2.0) [ 53 ], to visually represent the differences in RFC4 gene expression between tumor and normal tissue.…”