{'fraction_non_alphanumeric': 0.020017406440382943, 'fraction_numerical': 0.0, 'mean_word_length': 5.3535911602209945, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Loss of Aurora kinase signaling allows lung cancer cells to adopt an alternative cell cycle and form multinucleated polyploid giant cells that resist anti-mitotic drugs

Polyploid multinucleated (PP/MN) giant cancer cells are common in tumors and have been associated with resistance to cancer therapy, tumor relapse, malignancy, immunosuppression, metastasis, cancer stem cell production and modulation of the tumor microenvironment. However, the molecular mechanisms that cause these cells to form are yet known. In this study, we discover that Aurora kinases are synergistic determinants of a switch from the proliferative cell cycle to polyploid growth and multinucleation in lung cancer cell lines. When Aurora kinases are inhibited together, lung cancer cells uniformly grow into PP/MN giant cells. These cells have adopted an endocycle in which the genome replicates, mitosis is omitted and cells grow in size. Consequently, such cells continue to safely grow in the presence of antimitotic agents. These polyploid multinucleated cancer cells can re-enter the proliferative cell cycle and grow in cell number when the treatment is terminated.