{'fraction_non_alphanumeric': 0.02803129074315515, 'fraction_numerical': 0.009126466753585397, 'mean_word_length': 5.616379310344827, '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}}
Oleic acid-bound FABP7 drives glioma cell proliferation through regulation of nuclear lipid droplet formation.

Fatty acid-binding protein 7 (FABP7), one of the fatty acid (FA) chaperones involved in the modulation of intracellular FA metabolism, is highly expressed in glioblastoma and its expression is associated with decreased patients' prognosis. Previously, we demonstrated that FABP7 requires its binding partner to exert its function, and that a mutation in the FA binding site of FABP7 affects tumor biology. Here, we explored the role of FA ligand binding for FABP7 function in tumor proliferation, and examined the mechanism of FABP7 and ligand interaction in tumor biology. We discovered that among several FA treatment, oleic acid (OA) boosted cell proliferation of FABP7-expressing cells. In turn, OA increased FABP7 nuclear localization, and the accumulation of FABP7-OA complex in the nucleus induced the formation of nuclear lipid droplet (nLD), as well as increase in co-localization of nLD with promyelocytic leukemia (PML) nuclear bodies. Furthermore, OA increased mRNA levels of proliferation related genes in FABP7 expressing cells through histone acetylation. Interestingly, these OA-boosted functions were abrogated in FABP7 knockout cells and mutant FABP7-overexpressing cells. Thus, our findings suggest that FABP7-OA intracellular interaction may modulate nLD formation and the epigenetic status thereby enhancing transcription of proliferation-regulating genes, ultimately driving tumor cell proliferation.