@Article{biocell.2024.056374,
AUTHOR = {YAJUN CAO, SHUANG YIN, YIDAN FANG, JIEXIAN ZHOU, YOUTAN LIU},
TITLE = {Propofol suppressed cell proliferation through inhibition of SREBP1c-mediated <i>De novo</i> lipogenesis in colorectal cancer cells},
JOURNAL = {BIOCELL},
VOLUME = {48},
YEAR = {2024},
NUMBER = {12},
PAGES = {1773--1780},
URL = {http://www.techscience.com/biocell/v48n12/59146},
ISSN = {1667-5746},
ABSTRACT = { <b>Background:</b> <i>De novo</i> lipogenesis (<i>DNL</i>) is a critical event for the development of tumors, in the present work, we revealed the role of propofol in colorectal cancer (CRC) cell proliferation. <b>Methods:</b> Western blotting (WB), Real-time PCR, and luciferase combined with chromatin immunoprecipitation (ChIP) were used to identify the mechanism underlying propofol-modulated cell proliferation in CRC cells. <b>Results:</b> Herein, we showed that propofol suppressed cell proliferation, which was attributed to the inhibition of <i>DNL</i> characterized by reduced fatty acid synthase (FASN), acetyl-coA carboxylase alpha (ACCA), and stearoyl-coA desaturase-1 (SCD1) expression. Mechanically, propofol stimulation decreased sterol regulatory element-binding proteins-1c (SREBP-1c) mature and nuclear translocation, which further decreased SCD1 transactivation confirmed by luciferase and ChIP analysis, while no significant difference in total SREBP1c was observed. What’s more, supplementation of Monounsaturated fatty acid (MuFA) could reverse the inhibitory effect of propofol on cell proliferation. <b>Conclusion:</b> Taken together, these results suggested propofol modulated cell proliferation is dependent on SREBP1c-mediated <i>DNL</i>.},
DOI = {10.32604/biocell.2024.056374}
}