This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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.

No abstract

Background: Glioma is the most common brain tumor with poor prognosis all over the world. Anesthetics have been demonstrated to have important impacts on cell migration and invasion in different cancers. However, the underlying mechanism that allows anesthetics-mediated progression of glioma cells remains elusive. Methods: Sevoflurane (Sev), a class of common anesthetics, was used to expose to U87-MG and U251 cells. The expressions of microRNA-146b-5p (miR-146b-5p) and matrix metallopeptidase 16 (MMP16)were measured by quantitative real-time polymerase chain reaction or western blot. Transfection was performed in glioma cells with miR-146b-5p inhibitor, inhibitor negative control, MMP16 overexpression vector, empty vector, small interfering RNA against MMP16 or scramble. Cell migration and invasion were analyzed by the trans-well assay. The interaction between miR-146b-5p and MMP16 was explored by luciferase activity and RNA immunoprecipitation assays. Results: Sev treatment inhibited migration and invasion of glioma cells. The expression of miR-146b-5p was enhanced and MMP16 protein was decreased in glioma cells after exposure of Sev. Knockdown of miR-146b-5p or overexpression of MMP16 reversed Sev-induced inhibition of migration and invasion of glioma cells. Moreover, MMP16 was indicated as a target of miR-146b-5p and its silencing attenuated the regulatory role of miR-146b-5p abrogationin Sev-treated glioma cells. Conclusion: Sev impeded cell migration and invasion through regulating miR-146b-5p and MMP16 in glioma, indicating a novel theories foundation for the application of anesthetics like Sev in glioma.

BackgroundAcute pulmonary embolism (APE) can be life-threatening. Early detection is even more difficult for patients under general anesthesia as common symptoms are not available and the pathophysiological course of intra-operative APE is influenced by procedures of surgery and anesthesia, which makes patients under general anesthesia a distinctive group.Case presentationWe report a case of APE during orthopedic surgery under general anesthesia. A 64-year-old female with atrial fibrillation and surgical history of varicosity underwent total right hip replacement surgery under general anesthesia. No arterial or deep vein thrombosis (DVT) was found prior to the surgery, but APE still occurred intraoperatively. The sudden decrease in PETCO2 and increase in PaCO2 combined other clues raised the suspect of APE, which is further evidenced by transesophageal echocardiogram (TEE). Multidisciplinary consultation was started immediately. After discussion with the consultation team and communication with patient’s family members, anticoagulation therapy was started and IVC filter was placed to prevent PE recurrence. The patient went through the operation and discharged uneventfully 30 days later.ConclusionsPulmonary embolism is a rare and potentially high-risk perioperative situation, with a difficult diagnosis when occurs under anesthesia. The separation phenomenon of decrease in PETCO2 and increase in PaCO2 might be a useful and suggestive sign, enabling prompt management and therefore improving the prognosis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12871-017-0360-0) contains supplementary material, which is available to authorized users.