Open Access

ARTICLE

Propofol suppressed cell proliferation through inhibition of SREBP1c-mediated De novo lipogenesis in colorectal cancer cells

by YAJUN CAO^1,2,3,#, SHUANG YIN^1,2,#, YIDAN FANG⁴, JIEXIAN ZHOU^3,*, YOUTAN LIU^1,2,*

1 Department of Anesthesiology, Shenzhen Hospital, Southern Medical University, Shenzhen, 518000, China
2 The Third School of Clinical Medicine, Southern Medical University, Guangzhou, 510630, China
3 Department of Anesthesia, Zhuhai Center for Maternal and Child Health Care, Zhuhai, 519000, China
4 Department of Anesthesia, Zhuhai Doumen Maternal and Child Health Care Hospital, Zhuhai, 519000, China

* Corresponding Authors: JIEXIAN ZHOU. Email: ; YOUTAN LIU. Email:
# These authors contributed equally to this work

BIOCELL 2024, 48(12), 1773-1780. https://doi.org/10.32604/biocell.2024.056374

Received 21 July 2024; Accepted 12 October 2024; Issue published 30 December 2024

Abstract

Background: De novo lipogenesis (DNL) 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. Methods: 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. Results: Herein, we showed that propofol suppressed cell proliferation, which was attributed to the inhibition of DNL 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. Conclusion: Taken together, these results suggested propofol modulated cell proliferation is dependent on SREBP1c-mediated DNL.

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Keywords

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