Table 2.
ECM Protein | Role in PDAC | Implications in PDAC | References |
---|---|---|---|
Collagen |
The principal structural component of the ECM. Facilitates cell-ECM interactions. |
Increased collagen deposition, especially Type I collagen, can drive invasive behavior in PDAC. Associated with the promotion of cell proliferation and immunosuppression. |
|
Hyaluronan |
Another ECM molecule. Facilitates a physical barrier and a signaling molecule that influences the immune response. |
Accumulated HA leads to increased poor survival, and reduced T cell infiltration in the TME. Promotes infiltration and differentiation of tumor-associated macrophages. |
|
Matrix Metalloproteinases (MMPs) |
Enzymes that degrade ECM components. Involved in tissue inhibitors. |
Their overexpression can drive PDAC progression by degrading ECM and altering ECM dynamics. MMPs are key drivers of both tumor growth and metastasis during PDAC. |
|
Tissue Inhibitors of Metalloproteinases (TIMPs) |
Inhibit MMP activity. Regulate ECM turnover. |
Imbalance between TIMPs and MMPs can affect the integrity of the ECM in PDAC, influencing tumor behavior. | |
Fibronectin | Facilitates cell adhesion to the EMT. |
Elevated in PDAC and has been associated with tumor progression. Promotes cell proliferation and adhesion. |
|
Laminin |
Accumulate in the ECM. Facilitates cell migration and invasion. |
Alterations in laminin expression can affect PDAC cell adhesion and migration. |