Day 1 :
University of Crete, Greece
Eleni Petsalaki has completed her PhD at the age of 28 years at the University of Crete. She is currently a post doctoral research scientist in Dr George Zachos’ Cell Cycle and Division Lab at the University of Crete where she is investigating mechanisms of mitotic cell division in human cells. She has published 8 papers in peer reviewed journals including Nature Communications, Journal of Cell Biology, Journal of Cell Science and others, 2 review articles and 2 commentaries.
The mitotic spindle consists mainly of microtubules (MTs) and is essential for accurate distribution of chromosomes in the two daughter cells during cell division. Errors in spindle formation can lead to incorrect separation of chromosomes or unequal size of daughter cells, which are associated with carcinogenesis or developmental disorders. However, the molecular mechanisms of spindle formation are not fully understood. In the present study, we show for the first time that Chk1, a kinase involved in the cellular response to DNA damage, is essential for optimal density and effective polymerisation of the spindle MTs in human cells. Chk1 localises to the centrosomes (the main centers of MTs organization) in mitosis and phosphorylates β-tubulin in newly identified sites in vitro. Also, reduced microtubule density in cells without functional Chk1 is associated with formation of disorganized spindles. We suggest that Chk1 phosphorylates β-tubulin to promote optimal spindle MT polymerisation. These findings describe novel mechanisms that could protect against carcinogenesis and developmental disorders, through regulating formation of the mitotic spindle
University of Debrecen, Hungary
Eva Katona is graduated at the University of Debrecen in 2010, as medical biologist. She started her postgradual studies in the field of chondrogenic differentiation paralell with investigation of Ser/Thr phospatesis in human melanoma. In 2018, she started to studying the circadian clock of normal human epidermal pigment cells and melanoma cells, focusing on finding new strategies for resynchronization of the molecular clock of cancer cells.
Most of the cell functions show ~24 hour-periodic rhythm which is regulated by a 2-level endogenous rhythm-generator system. The clock machinery is composed of a central neural oscillator located in the brain, and peripheral clock systems found in different cells and tissues, where the expression of circadian clock genes is driven by a highly conserved transcription/translation feedback loop (TTFL).
It is hypothesised that cancer development and/or progression may correlate with the disruption of the circadian homeostasis of the cells. In case of melanoma, little is known about the elements, the function and the role of the biological clock. Recent studies suggest that re-synchronization of the circadian clock with special diet or pharmacological treatments may increase the positive effects of the antitumor therapies through decreasing cancer cell proliferation ability.
Based on the above, the aim of this research is to study the expression profile of the core molecular clock genes (BMAL1/2, CLOCK, CRY1/2, PER2/3, RevErba, RoRa) in WM35 melanoma cells and normal human epidermal melanocytes, as control cells. In addition to clock gene expression profiling, we show the alterations in the clock gene expression pattern upon re-synchronization with different methods i.e. serum shock or caloric restriction.
Our results suggest a differential regulation of the core molecular clock in melanoma cells compared to normal human epidermal melanocytes, which may have key implications in developing novel anti-cancer therapies.