Conclusion

The in vivo, in vitro and clinical studies reviewed here have shown that integrins are a promising therapeutic target in cancer progression and metastasis including prostate cancer. Since integrins are involved in mediating cell adhesion, deregulation of integrins leads to tumour invasion and metastasis. Studies have also found integrins to be involved in EMT in cancer progression. This occurs by either direct activation of the integrin and its signalling pathway or by activating the TGFß pathway and also mediating EMT transcription factors. However, studies on the involvement of integrins and the pathways involved in EMT is still very limited. Therefore, further studies are warranted to clarify the processes underlying in-tegrin involvement in EMT in cancer progression. To date, there are still no clinical studies investigating the effect on EMT of integrin inhibitors. These studies will improve our understanding of the integrin mediated EMT pathway and the effects on tumour metastasis. Since bone metastasis is the major cause of prostate cancer related death, targetting integrins using integrin inhibitors could potentially prove valuable in the prevention of the development of prostate cancer boney lesions.

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