{'fraction_non_alphanumeric': 0.02364864864864865, 'fraction_numerical': 0.02533783783783784, 'mean_word_length': 4.954773869346734, '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}}
Oct1 is required for mTOR-induced G1 cell cycle arrest via the control of p27Kip1 expression

Oct1 is a ubiquitously expressed transcription factor that is induced in response to DNA damage to modulate gene expression. Herein, Oct1 deficient mouse embryonic fibroblasts were used as a model to study the importance of Oct1 in cellular stress response. Cells lacking Oct1 kept proliferating and bypassed the G1 cell cycle arrest induced by glucose or amino acid starvation. Indeed, mTOR-mediated regulation of proliferation was abolished in Oct1-/- cells starved for glucose or amino acids and Oct1-/- cells were also insensitive to mTOR inhibition by rapamycin. Furthermore, in wild-type cells, Oct1 controls the transcription of the CDK inhibitor p27Kip1 downstream of the mTOR pathway and Oct1-null cells failed to upregulate p27Kip1 in response to rapamycin or glucose starvation. p27Kip1 is required for rapamycin or nutrient starvation-induced G1-arrest, as p27-/- fibroblasts were largely insensitive to rapamycin treatment or glucose starvation. Thus, Oct1 appears to be a critical mediator of the growth arrest induced by mTOR inhibition via the control of p27Kip1 expression.