Fig. 1.

A Illustration of the dynamic interconversion between cancer stem cells (CSCs) and non-CSCs. This figure illustrates the minor yet critical subpopulation of tumor mass known as CSCs. It visually elucidates the phenomenon of phenotypic plasticity that empowers both CSCs and non-CSCs to interchange states depending on various intrinsic and extrinsic cellular properties. Intrinsic factors include epigenetic changes that internally modulate cellular activities, while extrinsic factors encompass elements of the tumor microenvironment that externally influence the cells. The figure offers insight into the dynamic nature of cellular identity within tumor masses, emphasizing the impact of diverse cellular and microenvironmental factors on the CSC and non-CSC states. B Detailed overview of the regulatory network involving key transcription factors and molecules. This figure comprehensively depicts the transcription factors, including Snail1/Snail2, ZEB1/ZEB2, Twist, and LEF-1, whose expression is intricately modulated by multiple signaling pathways. It outlines the various regulatory molecules that can inhibit the functionality of these transcription factors, thus impacting cellular activities. The figure elaborates on the prevention of LEF-1 activation by GSK-3, which hinders its collaboration with β-catenin and also demonstrates GSK-3’s role in barring the stability and nuclear translocation of Snail1/Snail2. Additionally, the figure highlights the suppression of ZEB1/ZEB2 expression by the miR-200 family of miRNAs and the inhibition of GSK-3 and miR-200 by the kinase Akt, which is activated by most EMT signaling pathways