Cell Division and Cancer Laboratory
Cell Division and Cancer Laboratory
The aim of our research is to understand the molecular machinery that controls cell division to allow rational cancer chemotherapy.
Our work has identified key genes that control cell division and allowed us to see what they are doing in their normal setting: a live, developing animal. We developed tools to observe the cellular machinery that divides cells in two at the end of mitosis, and to find the genes that regulate this process.
This work is critical for an understanding of how normal growth works, but also to give us potential therapeutics that will allow us to block the uncontrolled cell division seen in cancer.
Cancers are cells that not only divide too much, but also usually divide unstably, gaining and losing chromosomes. This chromosomal instability is not seen in normal dividing cells, so it may be an ideal chemotherapy target - something that we can affect in the cancer without hurting normal cells.
Using the advantages of Drosophila genetics, we have screened for gene knockouts that can kill unstably dividing cells, but not normal ones. We have found several ways to specifically kill cells with chromosomal instability, including targeting the JNK pathway, centrosomes or cell metabolism. We are now working to explain why unstably dividing cells are sensitive to these processes, and how we can best target them.
Current Research Projects
To find out what is currently happening in the lab, and how you could be involved, check the current projects page.
Who to Contact
Z. Shaukat, D.Liu, R. Hussain, M. Khan and S. L. Gregory (2015). The role of JNK signaling in responses to oxidative DNA damage. Current Drug Targets 17:154-63 Impact 3.9 Citations: 3
A. Choo, L.V. O’Keefe, C-S. Lee, S. L. Gregory, Z. Shaukat, A. Collella, K. Lee, D. Denton, R. I. Richards (2015) Tumour suppressor WWOX moderates the mitochondrial respiratory complex.Genes Chromosomes and Cancer 54:745-61 Impact 4.0 Citations: 2
D.Liu, Z. Shaukat, R. Saint and S. L. Gregory (2015). Chromosomal instability triggers cell death via local signaling through the innate immune receptor Toll. Oncotarget 6:38552-65 Impact 6.4
D. Liu, Z. Shaukat, R. Hussain, M. Khan and S. L. Gregory (2015). Drosophila as a model for chromosomal instability.AIMS Genetics 2:1-12 Citations:1
Z. Shaukat, D. Liu and S. L. Gregory (2015). Sterile inflammation in Drosophila.Mediators of Inflammation 2015:369286. Impact 3.2 Citations: 2
Z. Shaukat, D. Liu, A. Choo, R. Hussain, L. O'Keefe, R.I. Richards, R.B. Saint, and S.L. Gregory (2015). Chromosomal instability causes sensitivity to metabolic stress. Oncogene 34 (31), 4044-4055 Impact 8.6 Citations: 7
H. Wong, Z. Shaukat, J-B. Wang, R. Saint and S. Gregory (2013). JNK signaling is needed to tolerate chromosomal instability. Cell Cycle 13:622-631 Impact 5.2 Citations: 5
Z. Shaukat, H. Wong, S. Nicolson, R. Saint and S. L. Gregory (2012). A screen for selective killing of cells with Chromosomal Instability induced by a spindle checkpoint defect. PLoS One 7(10):e47447 Citations:9
Z.I. Bassi, K.J. Verbrugghe, L. Capalbo, S. Gregory, E. Montembault, D.M. Glover and P.P. D’Avino (2011). Sticky/Citron Kinase maintains proper RhoA localization at the cleavage site during cytokinesis. Journal of Cell Biology Impact 9.6 Citations: 24
S. Ebrahimi, H. Fraval, M. Murray, R. Saint and S. L. Gregory (2010). Polo kinase interacts with RacGAP50C and is required to localize the cytokinesis initiation complex. Journal of Biological Chemistry 285:28667-28673. Impact 5.3 Citations: 11
S. L. Gregory, S. Ebrahimi, J. Milverton, W. H. Jones, A. Bejsovec and R. Saint (2008). Cell division requires a direct interaction between microtubule-associated RacGAP and the contractile ring component Anillin. Current Biology 18:25-29. Impact 11. Citations 104
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