Sevoflurane suppresses cell viability and invasion and promotes cell apoptosis in colon cancer by modulating exosome‑mediated circ‑HMGCS1 via the miR‑34a‑5p/SGPP1 axis

Abstract

As a novel halogenated hydroxyl ether-inhaled general anesthetic, sevoflurane has been reported to affect the progression of diverse human cancers. In the present study, we aimed to explore the functions and underlying mechanisms of sevoflurane in colon cancer. MTT assay, flow cytometric analysis and Transwell assay were conducted to evaluate cell viability, apoptosis and invasion, respectively. Western blot analysis was performed to determine the protein level of sphingosine-1-phosphate phosphatase 1 (SGPP1). The morphology and size of exosomes were analyzed by TEM and NTA. The levels of circular RNA 3-hydroxy-3-methylglutaryl-CoA synthase 1 (circ-HMGCS1), microRNA (miR)-34a-5p and SGPP1 mRNA were examined by RT-qPCR. Dual-luciferase reporter and RNA RIP assays were utilized to explore the interaction between miR-34a-5p and circ-HMGCS1 or SGPP1. A murine xenograft model was established to investigate the effect of circ-HMGCS1 in vivo . As a result, it was determined that sevoflurane suppressed cell viability and invasion and induced apoptosis in colon cancer in a dose-dependent way. Exosomal circ-HMGCS1 was increased in the serums and cells of colon cancer patients. Circ-HMGCS1 was downregulated by sevoflurane treatment in colon cancer cells and circ-HMGCS1 overexpression could restore the effect of sevoflurane on colon cancer cell development. miR-34a-5p was a target of circ-HMGCS1 and miR-34a-5p inhibition reversed the effect of circ-HMGCS1 silencing on colon cancer cell progression. Moreover, circ-HMGCS1 knockdown suppressed SGPP1 expression via sponging miR-34a-5p. Knockdown of circ-HMGCS1 blocked tumor growth in vivo . In conclusion, sevoflurane inhibited colon cancer progression by modulating the exosome-transmitted circ-HMGCS1/miR-34a-5p/SGPP1 axis.

Wnt/β-Catenin Signaling as a Driver of Hepatocellular Carcinoma Progression: An Emphasis on Molecular Pathways

“…Sevoflurane (Sevo) is a volatile anesthetic agent that has shown anti-tumor activity via apoptosis induction, triggering cell cycle arrest and metastasis inhibition. 247 Sevo is able to promote miRNA-29a expression to down-regulate Dnmt3a, impairing HCC growth. 248 In HCC cells, Sevo decreases expression level of miRNA-25-3p to induce PTEN signaling.…”

Exosomal miR-486-5p derived from human placental microvascular endothelial cells regulates proliferation and invasion of trophoblasts via targeting IGF1

“…Previous research has confirmed that exosomes play a role in multiple conditions, including PE [11,25,26]. Furthermore, trophoblast cell growth inhibition, and dysregulation of miRNAs are involved in the progression of PE [27,28].…”

“…Exosomes are a type of extracellular vesicle (EV), with diameter ranging from 40 to 100 nm; exosomes are secreted by cells, and transfer signal molecule to targeted cells [11]. In addition, exosomes play key roles in the progression of multiple diseases [12,13].…”

Sevoflurane inhibits malignant progression of colorectal cancer via hsa_circ_0000231-mediated miR-622

“…For example, Li and his colleagues indicated Sev repressed cell proliferation and metastasis by decreasing circ_0002755 and circ_0012129 expression in glioma [ 14 ]. He et al revealed that Sev restrained cell proliferation and induced cell apoptosis via controlling circ-3-hydroxy-3-methylglutaryl-CoA synthase 1 (circ-HMGCS1) in colon cancer [ 15 ]. In this study, we found that circ_0000231 (hsa_circ_0000231) was increased in CRC specimen and cell lines, but decreased in Sev-treated CRC cells.…”