Clusterin is a conserved
glycoprotein that has been characterized from almost all human tissues and fluids and plays a key role in cellular stress response and survival. Recently, research efforts have been contributed to explore the function of
Clusterin in
cancer metastasis, which is particularly important to design the strategies for treating metastatic patients. Evidence collected has demonstrated that
Clusterin is overexpressed in
tumor metastatic patients and experimental
metastasis models. Specifically,
Clusterin has been shown to have the role in anti-apoptotic capacities, development of
therapy resistance and induction of epithelial-mesenchymal transition, all associated with
cancer metastasis. Inhibition of
Clusterin is known to increase the cytotoxic effects of chemotherapeutic agents and improves advanced
cancer patients survival in clinical trials. Our unpublished data have demonstrated that
Clusterin is overexpressed in
bladder cancer and
metformin, a well-known metabolism modulator specifically targets
Clusterin by inhibiting migration of
bladder cancer cells. In this review, we provide a general view of how
Clusterin modulates
cancer metastasis and update current understanding of detailed molecular mechanisms underlying of
Clusterin for developing
cancer management in future.