Table 1 Integrin functions in different solid cancer types

β1

Src/AKT

Lung

Promotes chemoresistance against EGFR inhibitor Erlotinib

[35]

α2β1

Collagen type I

Prostate

Promotes prostate cancer cell invasion and skeletal metastasis

[36]

CDH-17

Colon

Interacts with CDH17 to induce FAK and Ras activation and thus promotes tumor growth and liver metastasis

[37]

α3β1

Rho/Yap

CRPC

Suppresses anchorage-independent growth and metastasis

[38]

α6

AKT/ERK

Breast

Expresses highly in breast cancer vs. normal cells and enhances radiotherapy resistance

[39]

α7

Laminin

Glioblastoma

Correlates negatively with patient survival and promotes growth and invasiveness of CSCs

[40]

α9β1

β-catenin/E-cadherin

Lung

Promotes EMT, tumor growth, vasculogenesis and metastasis

[41]

α10β1

Collagen and Laminin

Glioblastoma

Upregulates in both glioblastoma tissue and cells, correlates with high-grade gliomas, and promotes cell proliferation and migration

[42]

β3

TGFβ

NSCLC

Accelerates cancer cell adhesion to lymphatic endothelium after TGF-β exposure, and combined targeting of β3 integrin and TGFβ reduces lymph node metastasis

[43]

αvβ3

OPN/FAK

NSCLC

Enhances cell proliferation and EGFR-TKI resistance

[44]

Survivin

CRPC

Promotes anchorage-independent cell growth and enhances IR resistance via stabilization of Survivin

[45]

KRAS/RalB

Lung/Breast/ Pancreas

Recruits KRAS and RalB to activate TBK1 and NF-κB, leading to enhanced stemness and RTK inhibitor resistance

[46]

αvβ6

MMP9

SCC

Promotes invasion in an MMP9-dependent manner

[31]

JNK1/Survivin

CRPC

Promotes anchorage-independent growth and cancer progression via activation of androgen receptor

[28]

α6β4

BNIP3L

TNBC

Induces BNIP3L-dependent mitophagy and lactate production in CAFs, which in turn promotes EMT, proliferation and invasion

[47]

β8

ECM

PDAC

Regulates positively cancer cell radiochemoresistance, intracellular vesicle trafficking, and autophagy

[48]