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Gao, Sizhen

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Gao

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Sizhen

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Gao, Sizhen
Author's Publications: search.filters.isAuthorOfPublication.18998b20-e5d1-413b-b9fc-a975d0409453

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    Characterization of twenty-five ovarian tumour cell lines that phenocopy primary tumours
    (Nature Pub. Group, 2015) Ince, Tan A.; Sousa, Aurea D.; Jones, Michelle A.; Harrell, J. Chuck; Agoston, Elin S.; Krohn, Marit; Selfors, Laura; Liu, Wenbin; Chen, Ken; Yong, Mao; Buchwald, Peter; Wang, Bin; Hale, Katherine S.; Cohick, Evan; Sergent, Petra; Witt, Abigail; Kozhekbaeva, Zhanna; Gao, Sizhen; Agoston, Agoston; Merritt, Melissa A.; Foster, Rosemary; Rueda, Bo; Crum, Christopher; Brugge, Joan; Mills, Gordon B.
    Currently available human tumour cell line panels consist of a small number of lines in each lineage that generally fail to retain the phenotype of the original patient tumour. Here we develop a cell culture medium that enables us to routinely establish cell lines from diverse subtypes of human ovarian cancers with >95% efficiency. Importantly, the 25 new ovarian tumour cell lines described here retain the genomic landscape, histopathology and molecular features of the original tumours. Furthermore, the molecular profile and drug response of these cell lines correlate with distinct groups of primary tumours with different outcomes. Thus, tumour cell lines derived using this methodology represent a significantly improved platform to study human tumour pathophysiology and response to therapy.
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    DIAPH3 Governs the Cellular Transition to the Amoeboid Tumour Phenotype
    (WILEY-VCH Verlag, 2012) Hager, Martin H; Morley, Samantha; Bielenberg, Diane; Gao, Sizhen; Morello, Matteo; Holcomb, Ilona N; Liu, Wennuan; Mouneimne, Ghassan; Demichelis, Francesca; Kim, Jayoung; Solomon, Keith R.; Adam, Rosalyn; Isaacs, William B; Higgs, Henry N; Vessella, Robert L; Di Vizio, Dolores; Freeman, Michael R.
    Therapies for most malignancies are generally ineffective once metastasis occurs. While tumour cells migrate through tissues using diverse strategies, the signalling networks controlling such behaviours in human tumours are poorly understood. Here we define a role for the Diaphanous-related formin-3 (DIAPH3) as a non-canonical regulator of metastasis that restrains conversion to amoeboid cell behaviour in multiple cancer types. The DIAPH3 locus is close to RB1, within a narrow consensus region of deletion on chromosome 13q in prostate, breast and hepatocellular carcinomas. DIAPH3 silencing in human carcinoma cells destabilized microtubules and induced defective endocytic trafficking, endosomal accumulation of EGFR, and hyperactivation of EGFR/MEK/ERK signalling. Silencing also evoked amoeboid properties, increased invasion and promoted metastasis in mice. In human tumours, DIAPH3 down-regulation was associated with aggressive or metastatic disease. DIAPH3-silenced cells were sensitive to MEK inhibition, but showed reduced sensitivity to EGFR inhibition. These findings have implications for understanding mechanisms of metastasis, and suggest that identifying patients with chromosomal deletions at DIAPH3 may have prognostic value.