Review Article

Alterations in Cell-Extracellular Matrix Interactions during Progression of Cancers

Table 1

Various integrins in association with different ligands to induce different signaling pathways in generation of tumor and metastasis.

Integrin typeInteracting ECM proteinActivated signaling cascadeTumor/metastasisReference

α3β1LamininMMP9 and oncogenic Ras, VEGF, FAK-paxillin signaling cascadeInvasion in keratinocytes, Induces angiogenesis,
Human hepatoma cells
[33, 34]
α6β1Laminin Urokinase plasminogen activator and MMP-2, PI3Kinase, SrcTumor invasion in pancreatic cells[35, 36]
α7β1Laminin Rho-A signaling cascadeInvasion in breast cancer[37]
α2β1, α1β1, α10β1, αIIβ1CollagenFAK and src signalingInvasion of melanoma cells, cancer progression, and invasion of lung adenocarcinoma[38, 39]
αvβ1, αvβ6, αvβ3Vitronectin, syndican, thromospondin-1MMP9, urokinase signaling, MEK/Erk/NF- B, PKCa, FAKMetastatic breast Cancer, pancreatic, cervical, colon, lung/liver metastasis[4042]
α9β1CCN3, osteopontin Src, P130 Cas, Rac, NOS signalingMetastatic potential[43]
αIIb3, αvb3Von Willebrand factor Interacts with thrombospondin-1 and induces VEGF/FGF signalingBreast cancer[44, 45]
α5Fibronectin FAK, ERK, PI-3 K, ILK, and nuclear factor-kappa B -Metastatic lung and cervical cancer[46, 47]
αLβ2Intercellular cell adhesion moleculesBreast cancer[1]