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Biomedicine researchers demonstrate the relationship between the atypical cycline alterations and the onset of cancer
A study led by Dr Eva Quandt and Dr Nuria Masip, researchers in the area of Biomedicine under the Department of Basic Sciences, has been published in the prestigious journal Molecular Oncology and provides new information regarding the atypical cyclin CCNI
With the title “CDK6 is activated by the atypical cyclin I to promote E2F-mediated gene expression and cancer cell proliferation,” the article is part of one of the lines of work the research group GRC-From Cell Metabolism to Metabolic Diseases, iwith participation of researchers Eva Quandt, Núria Masip, Sara Hernández, Abril Sánchez, Laura Gasa, Ainhoa Fernández, Sara Plutta, Joan Marc Martínez, Samuel Bru, Pau M. Muñoz, and Alberto Villanueva and coordinated by Dr Mariana Ribeiro and Dr Josep Clotet.
The research, published in the journal Molecular Oncology, studies how alterations in the proteins that control cell division are correlated with the onset of cancer. Specifically, the research focuses on atypical cyclines, which, despite being discovered years ago, are still a group of poorly characterized proteins and on which little information is available. The project provides new information regarding one of these atypical cyclines, cyclin I (CCNI).
As explained by the researchers, this research has a great scientific impact since it demonstrates the importance of cyclin I in the complex machinery of cell cycle control and its role as a potential oncogenic driver. Moreover, the study also revealed that these effects of CCNI are activated through the cell-division protein kinase 6 (CDK6). This opens up new strategies when using current CDK6 inhibitor drugs in cancer treatments and also opens the door to the possibility of designing new therapeutic strategies for this disease.
Within the context of World Cancer Day, researcher Nuria Masip explains in this video the line of research in which the Atypical cyclins research group to which she belongs is working: