TABLE 3.
The role of EMT-related pathways in colorectal cancer.
| Pathways | Altered mechanism | Role in CRC | Ref. |
|---|---|---|---|
| TGF-β/SMAD | Aberrant activation by LINC00941 upregulation and/or HAPLN1 reduction | Principal EMT activator. Crosstalk with other pathways (e.g., Wnt/β-catenin) | Wang et al. (2021); Wu et al. (2021b) |
| NF-κB | Increased production of inflammatory and anti-apoptotic mediators | Links inflammation to cancer development | Jurjus et al. (2016) |
| Wnt/β-catenin | APC inactivation and specific transcriptional signature induction | Onset and progression | Bian et al. (2020) |
| Notch | Increased activation by altered MMP9 activity | Modulation of tumor microenvironment | Walter et al. (2020) |
| ERK pathway | Activation of EMT-inducing transcription factors; regulation cell adhesion molecules and MMPs | Progression and invasion | Wang et al. (2017); Xu et al. (2018); Ni et al. (2023) |
| Hedgehog | Positively regulated by increased GLI1 and POU4F2 expression | EMT genes expression and dedifferentiation | Centelles (2012); Guo et al. (2021) |
| HIF | Increased Ascl2 expression (blocked by miR-200b); inhibition by miR-206; induction of angiogenic factors like VEGF | Angiogenesis and progression | Shang et al. (2017); Xu et al. (2018) |
| PI3K/Akt/mTOR | Regulation of EMT-related transcription factors; protein translation and synthesis; crosstalk with autophagy | Cell growth, angiogenesis and metastasis | Liao et al. (2022); Wu et al. (2023) |