Open Access

ARTICLE

Propofol inhibits cells migration and invasion via HOTAIR/miR-93/HIF-1α-mediated lactate secretion in colon cancer

RUONAN GU^1,2, WENJING GUO², WENYANG WANG¹, GUIHUAN LI¹, XIAOJU LAI¹, ZHIBIN HUANG¹, WANLU ZHAO¹, ZHICONG WU¹, HUA CHEN¹, WENYANG LUO¹, FANGYIN ZENG^3,*, FAN DENG^1,*

1 Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China
2 Department of Anesthesiology, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China
3 Department of Clinical Laboratory, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, 510920, China

* Corresponding Authors: FANGYIN ZENG. Email: ; FAN DENG. Email:

(This article belongs to this Special Issue: Regulatory, Therapeutic and Diagnostic Associations of miRNA in Emerging Diseases)

BIOCELL 2021, 45(6), 1585-1599. https://doi.org/10.32604/biocell.2021.017016

Received 20 April 2021; Accepted 18 June 2021; Issue published 01 September 2021

Abstract

Propofol, a common intravenous anesthetic used in clinical, has been shown to regulate cells proliferation, inflammation, angiogenesis and metastasis as well as exerting anti-cancer effect in several different types of cancer. However, the functions and mechanisms of propofol in lactate secretion and invasion of cancer cells remain unknown. The primary aim of this study was to investigate the role of propofol in cells migration and invasion of colon cancer (CRC). Scratches assay, Transwell assay were used to detect colon cells migration and invasion. Real-time Quantitative Polymerase Chain Reaction (RT-qPCR), Western blotting were utilized to detect the expression of related molecules. Dual-luciferase assay was performed to identify transcriptional activity of target genes, RNA pull-down assay was used to confirm the interactions of RNAs. Results indicated that propofol inhibited cell migration and invasion through suppressing lactic acid production in CRC. Moreover, propofol reduced lactic acid production by down-regulating the expression of hypoxia inducible factor-1α (HIF-1α) and monocarboxylate transporter 4 (MCT4). In addition, propofol inhibited the expression of HIF-1α and cells migration/invasion via suppressing the interaction of HOX transcript antisense RNA (HOTAIR) with miR-93. The present study indicated that propofol inhibited colon cancer cell migration and invasion by reducing lactic acid production and the expression of HIF-1α and MCT4 via HOTAIR/miR-93 axis. These data may provide potential metabolic targets for CRC treatment.

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