Protein AP1 makes DNA in the cell nucleus more accessible during oncogenesis via the Kras pathway - potential target for cancer treatment
Cancers are often linked to mutations in genes known as oncogenes, typically involved in regulating cell division. Among these, the gene Kras is implicated in over 25% of cancers, particularly in the lung, colon and pancreas. Recent research, focusing on lung tissue, reveals that mutated Kras induces cells to multiply by orchestrating structural rearrangements of chromatin, the carefully-packaged bundle of DNA and proteins in cell nuclei. It does so by harnessing a protein complex, AP1, which reshapes chromatin, making some sections of DNA more accessible. Similar mechanisms operate in two types of cells involved in lung cancer, club cells and alveolar cells, but club cells (pictured in culture, in green) also change their nature, expressing proteins (highlighted in red) more typical of alveolar cells. Inhibiting AP1 prevents chromatin remodelling and cell proliferation in cultured Kras mutant cells, suggesting a potential new route for tackling notoriously hard to treat Kras-related cancers.
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