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  Galectin function and therapeutic potential in cancer progression and metastasis.


   Department of Cellular and Molecular Physiology

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  Prof LG Yu  Applications accepted all year round  Self-Funded PhD Students Only

About the Project

Galectins are a family of 15 human galactoside-binding proteins. Overexpression of members of galectins (e.g. galectin-1 and -3) are common features in various types of cancers (e.g. colorectal, lung, breast, prostate, pancreatic and melanoma) and are increasingly recognized to play an important role in cancer progression and metastasis through divergent mechanisms. Targeting the galectin-mediated actions in cancer is believed to be a promising therapeutic strategy for cancer treatment. Recent studies in our laboratory have revealed that the levels of several galectin members are markedly increased (up to 30-fold) in the bloodstream of cancer patients and the increased circulation of those galectins promote circulating tumour cell metastatic spread to remote organs. This project will investigate the molecular mechanism of galectin-mediated metastasis promotion and also assess strategies and effectiveness of blocking galectin-mediated actions to reduce cancer cell activities and metastasis with novel galectin-binding inhibitors. Various techniques in cancer cell biology, molecular biology, biochemistry and structural biology will be used in the study. The student will join a dynamic research team composed of postdoctoral researchers and PhD students in a stimulating and multi-disciplinary environment. The student will also be provided with opportunities to obtain training of transferable skills by enrolling various training programmes run by the University of Liverpool.

Applications accepted all year round but fee bursary might be available for applications received by the end of April 2017.

Informal enquiries are welcome to Professor Lu-Gang Yu, Email: [Email Address Removed]


Funding Notes

This PhD studentship opens for sponsored and self-funded students from UK, EU and overseas. Candidates with the right qualifications, aptitude and desire, and with secured funding (eg from their government or from their own finance) will be considered.

References

1. Duckworth CA, Guimond SE, Sindrewicz P, Hughes AJ, French NS, Lian LY, Yates EA, Pritchard DM, Rhodes JM, Turnbull JE, Yu LG. (2015). Chemically modified, non-anticoagulant heparin derivatives are potent galectin-3 binding inhibitors and inhibit circulating galectin-3-promoted metastasis. Oncotarget 6:23671-23687.
2. Chen C, Duckworth CA, Zhao Q, Pritchard DM, Rhodes JM, Yu LG. (2013). Increased circulation of galectin-3 in cancer induces secretion of metastasis-promoting cytokines from blood vascular endothelium. Clinical Cancer Research 19:1693-704.
4. Barrow H, Guo X, Wandall HH, Pedersen JW, Fu B, Zhao Q, Chen C, Rhodes JM, Yu LG. (2011). Serum galectin-2, -3, -4 and -8 are greatly increased in colon and breast cancer patients and promote cancer cell adhesion to blood vascular endothelium. Clinical Cancer Research 17:7035-46.
5. Zhao Q, Barclay M, Hilkens J, Guo X, Barrow H, Rhodes JM, Yu LG. (2010). Interaction between circulating galectin-3 and cancer-associated MUC1 enhances tumour cell homotypic aggregation and prevents anoikis. Molecular Cancer 9:154
6. Zhao Q, Guo X, Stone P, Nash G, Hilkens J, Rhodes JM, Yu LG. (2009). Circulating galectin-3 promotes metastasis by modifying MUC1 localization on cancer cell surface. Cancer Research 69:6799-806.

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