Six of the same signalling pathways are involved in the process of  EMT as are driving Cancer Stem Cells (CSC's):

1) Transforming Growth Factor-beta (TGF-β) pathway: TGF-β signalling plays a critical role in EMT induction. Activation of TGF-β pathway triggers a cascade of events that leads to the loss of epithelial characteristics and acquisition of mesenchymal traits.

2) Wnt/β-catenin pathway: The Wnt signalling pathway is involved in various cellular processes, including EMT. Activation of Wnt pathway can stabilise β-catenin, which translocates into the nucleus and regulates the expression of EMT-associated genes.

3) Notch pathway: The Notch signalling pathway is involved in cell fate determination and tissue development. Dysregulation of the Notch pathway has been associated with EMT and cancer progression.

4) Hedgehog (Hh) pathway: The Hh pathway plays a crucial role in embryonic development and tissue homeostasis. Aberrant activation of the Hh pathway has been implicated in promoting EMT and cancer metastasis.

5) PI3K/Akt/mTOR pathway: The PI3K/Akt/mTOR pathway is involved in cell survival, growth, and proliferation. Dysregulation of this pathway can promote EMT and cancer progression.

6) Nuclear factor-kappa B (NF-κB) pathway: The NF-κB pathway regulates inflammation and immune responses. Activation of NF-κB signaling has been associated with EMT induction and metastasis.

7) RTK pathways, the other important signalling pathways in the EMT process:
In regards to EMT the Receptor Tyrosine Kinase (RTK) pathways are also up-regulated and need inhibiting: Various RTK pathways, such as epidermal growth factor receptor (EGFR), hepatocyte growth factor receptor (MET), and fibroblast growth factor receptor (FGFR), can activate downstream signalling cascades that contribute to EMT. Berberine, Curcumin and Genistein, has all been reported to inhibit EGFR, hepatocyte growth factor receptor (MET) and FGFR signalling.

These signalling pathways are interconnected and often exhibit cross-talk, creating a complex network that regulates EMT and cancer progression. The specific involvement of these pathways may vary depending on the cancer type and context.

EMT is a process in which epithelial cells lose their characteristics and acquire mesenchymal traits, promoting increased motility and invasiveness. CSCs, on the other hand, are a subset of cancer cells with stem cell-like properties, including self-renewal and differentiation capabilities.

With EMT the following protein markers increase and they can activate the above signalling pathways and gene expression programs that contribute to both EMT and CSC phenotypes: Vimentin, Fibronectin, Snail 1 (Snail), Snail 2 (Slug), Twist, FOX C2, SOX 10, MMP-2, MMP-3, MMP-9, N-cadherin. These protein markers that we need more of decrease: E-cadherin, Desmoplakin, Cytokeratin, Occludin

Functional markers observed with EMT: Increased migration, increased invasion, increased scattering, elongation of cell shape, resistance to anoikis*

*Anoikis is a programmed cell death occurring upon cell detachment from the correct extracellular matrix, thus disrupting integrin ligation. It is a critical mechanism in preventing dysplastic cell growth or attachment to an inappropriate matrix.