Differential role of intravenous anesthetics in colorectal cancer progression: implications for clinical application

Deng, Feihong; Ouyang, Ming-Wen; Wang, Xiaofei; Yao, Xueqing; Chen, Ye-ming; Tao, Tao; Sun, Xuegang; Xu, Li; Tang, Jing; Zhao, Liang

doi:10.18632/oncotarget.12800

Cited by 32 publications

(31 citation statements)

References 36 publications

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“…Propofol (2, 6-diisopropylphenyl) is a widely used agent during the induction and maintenance of anesthesia. It has been revealed recently that propofol exerts antitumor effects against some malignancies via inhibition of cell viability and the dispersion and invasion capacity of cancer cells [20-22]. However, its effect on glucose metabolism in cancer cells is not well understood.…”

Section: Introductionmentioning

confidence: 99%

Propofol Disrupts Aerobic Glycolysis in Colorectal Cancer Cells via Inactivation of the NMDAR-CAMKII-ERK Pathway

Chen

Sun

et al. 2018

Cell Physiol Biochem

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Background/Aims: To investigate the effect of propofol on glucose metabolism in colorectal cancer cells and in an in vivo xenograft model. Methods: Glucose metabolism was assessed by measuring the extracellular acidification rate in HT29 and SW480 colorectal cancer cells. Quantitative real-time PCR and western blot analyses were used to detect mRNA and protein levels, respectively. Intracellular calcium was assessed by using a Fluo-3 AM fluorescence kit. Micro-positron emission tomography/computed tomography (microPET/CT) imaging was used to analyze glucose metabolism in the tumors of the xenograft model. Results: Propofol exposure induced a dose-dependent decrease of aerobic glycolysis in HT29 and SW480 colorectal cancer cells. MicroPET/CT indicated that propofol also inhibited ¹⁸F-FDG uptake in the xenograft model. In addition, hypoxia-inducible factor 1α (HIF1α) was also reduced by propofol dose-dependently. Propofol repressed the NMDAR-CAMKII-ERK pathway to inactivate HIF1α and therefore reduced glycolysis. Conclusion: Propofol inhibited aerobic glycolysis in colorectal cancer cells through the inactivation of the NMDAR-CAMKII-ERK pathway, which may facilitate a better understanding of the use of propofol in the clinical setting.

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Section: Introductionmentioning

confidence: 99%

Propofol Disrupts Aerobic Glycolysis in Colorectal Cancer Cells via Inactivation of the NMDAR-CAMKII-ERK Pathway

Chen

Sun

et al. 2018

Cell Physiol Biochem

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“…The volatile anesthetics upregulate HIFs [10][11][12][13][14][15][16] and HIF overexpression is associated with an unfavorable prognosis in breast cancer [57,58]. HIF-1α has been found to promote EMT in many human malignancies leading to increased cancer aggressiveness [59].…”

Section: Discussionmentioning

confidence: 99%

“…Other anesthetics (e.g. propofol and etomidate) are able to stimulate the EMT initiation through the increment of mesenchymal markers expression [15]. Volatile anesthetics (e.g.…”

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confidence: 99%

“…Volatile anesthetics (e.g. halothane, isoflurane, sevoflurane) have been implicated in angiogenesis and immunosuppression, induced apoptosis of immune competent cells (NK cells and T-lymphocytes), but also have a promoting effect on tumor metastasis [10][11][12][13][14][15][16]. Although sevoflurane is nowadays the most frequently used inhaled anesthetic, its direct influence on cancerous cells is mainly unknown.…”

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confidence: 99%

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Sevoflurane Modulates Akt Isoforms In Triple Negative Breast Cancer Cell Line

Tiron

Postu

Vacarean-Trandafir

et al. 2020

Preprint

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Background: Triple negative breast cancer (TNBC) is a highly aggressive tumor, associated with high rates of early distant recurrence and short survival times and treatment may require surgery, and thus anesthesia. The effects of anesthetic drugs on cancer progression are under scrutiny, but published data are controversial and the involved mechanisms unclear. Anesthetic agents have been shown to modulate several molecular cascades, including PI3K/AKT/mTOR. AKT isoforms are frequently amplified in various malignant tumors and associated with malignant cell survival, proliferation and invasion. Their activation is often observed in human cancers and is associated with decreased survival rate. Certain anesthetics are known to affect hypoxia cell signalling mechanisms by upregulating hypoxia-inducible factors (HIFs). Methods: MCF-10A and MDA-MB 231 cells were cultivated and CellTiter-Blue® Cell Viability assay, 2D and 3D matrigel assay, immunofluorescence assays and gene expressions were performed after exposure to different sevoflurane concentrations.Results: Sevoflurane exposure of triple negative breast cancer cells results in morphological and behavioral changes. Sevoflurane differently influences the AKT isoforms expression in a time-dependent manner, with an important early AKT3 upregulation. The most significant effects occur at 72 hours after 2mM sevoflurane treatment and consist in increased viability, proliferation and aggressiveness and increased vimentin and HIF expression. Conclusion: Sevoflurane exposure during surgery may contribute to cancer recurrence via AKT3 induced EMT and by all three AKT isoforms enhanced cancer cell survival and proliferation.

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“…Previous studies have suggested that it has an anti-cancer effect in addition to its anesthetic effect. Research has demonstrated that propofol could inhibit cancer cell proliferation, migration and invasion, and thus exert anti-tumor function (27)(28)(29)(30). Previous studies have identified that propofol could inhibit the development of numerous cancer types, including pancreatic (31), breast (32), colon (33), gastric (34) Figure 2.…”

Section: Primer (5'-3') ---------------------------------------------mentioning

confidence: 99%

Effects of propofol on human cholangiocarcinoma and the associated mechanisms�

et al. 2018

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Cholangiocarcinoma (CCA) is the most common type of biliary duct malignancy. Propofol is a fast-acting intravenous anesthetic, which also exerts an anti-cancer effect. The aim of the current study was to explore the effects of propofol on human CCA and the associated mechanisms in vitro. The results indicated that as concentration (0, 1, 5 and 10 µg/ml) of propofol and treatment time (24, 48 and 72 h) increased, the cell inhibition rate of human CCA QBC939 cells increased. Furthermore, treatment with various concentrations of propofol for 48 h resulted in a decrease in migration and invasion capacity in QBC939 cells. Propofol also induced the apoptosis of QBC939 cells and cell cycle arrest in G1 phase. Propofol treatment increased the expression level of Bax and decreased that of Bcl-2. In addition, the effects of propofol on gene expression were evaluated, including Wnt3α, β-catenin, Snail1 and c-myc in the Wnt/β-catenin signaling pathway. It was identified that as the concentration of propofol increased, the expression of these genes decreased. In conclusion, the current results indicate that propofol is a promising therapeutic agent for the treatment of CCA.

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Differential role of intravenous anesthetics in colorectal cancer progression: implications for clinical application

Cited by 32 publications

References 36 publications

Propofol Disrupts Aerobic Glycolysis in Colorectal Cancer Cells via Inactivation of the NMDAR-CAMKII-ERK Pathway

Propofol Disrupts Aerobic Glycolysis in Colorectal Cancer Cells via Inactivation of the NMDAR-CAMKII-ERK Pathway

Sevoflurane Modulates Akt Isoforms In Triple Negative Breast Cancer Cell Line

Effects of propofol on human cholangiocarcinoma and the associated mechanisms�

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