Effects of propofol on cancer development and chemotherapy: Potential mechanisms

Jiang, Sufang; Liu, Ya; Huang, Liyi; Zhang, Fuzhen; Kang, Ran

doi:10.1016/j.ejphar.2018.04.009

Cited by 89 publications

(66 citation statements)

References 75 publications

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“…The effects of propofol differ in various cell types due to the activation or inhibition of different signaling pathways (36). However, since ROS-dependent intrinsic apoptosis is generally mediated by MAPK (37), the present study examined the activation of the NF-κB and MAPK/p38/ERK/JNK signaling pathways, which have been reported to be crucial for CoCl 2 -induced apoptosis of BV2 (18) and HK2 cells (38).…”

Section: Discussionmentioning

confidence: 98%

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

et al. 2020

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Propofol is a widely used intravenous anesthetic shown to exert a cardioprotective role against oxidative stress and ischemia/reperfusion injury in rat cardiac H9c2 cells. However, the regulatory mechanisms and functions of propofol in human cardiomyocytes remain unknown. The present study chemically induced hypoxia with cobalt chloride (CoCl 2 ) to mimic cardiomyocyte ischemic injury in human cardiac AC16 and HCM cells. To investigate its underlying mechanisms, propofol was added to the cells before the chemical hypoxia phase. The present results suggested that, in response to hypoxia, mitochondrial membrane potential was lost, and cardiomyocyte viability and superoxide dismutase levels decreased. However, the present results showed that reactive oxygen species and malondialdehyde levels increased. The present results suggested that these effects were significantly reversed following propofol treatment. Additionally, the present results suggested that the protective effect of propofol against CoCl 2 -induced injury may be inhibited by the activation of the JNK signaling pathways. The present results indicated that propofol pre-treatment inhibited CoCl 2 -induced myocardial injury by preventing mitochondrial dysfunction, which may be partially due to the activation of the JNK signaling pathways. Therefore, propofol may exert anti-oxidative effects in human cardiac cells. The present results suggested that propofol may be used as a treatment for oxidative stress-related cardiac disorders.

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Section: Discussionmentioning

confidence: 98%

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

et al. 2020

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“…4 Par exemple, dans une des premières études sur le sujet, il a été démontré que le propofol promouvait la cytotoxicité de la cellule tueuse naturelle (natural killer), 5 laquelle pourrait combattre la dissémination cancéreuse; des études plus récentes de plus grande envergure n'ont toutefois pas confirmé cette hypothèse. 6 Des études supplémentaires ont également démontré que le propofol possédait certaines propriétés inhibitrices sur la cyclo-oxygénase et le facteur HIF-1a induit par l'hypoxie, ainsi que des propriétés de réduction de la motilité et de l'invasion des cellules cancéreuses 7 ; toutes ces propriétés pourraient minimiser l'activation des voies de progression du cancer. À l'inverse, les anesthésiques volatils peuvent provoquer l'activation de facteurs de croissance insulinomimétiques (ILGF) et du HIF-1a.…”

Section: Les Anesthésiologistes Peuvent-ils Avoir Un Impact Sur Les Punclassified

“…4 For example, propofol was shown in an early study to promote natural killer cell cytotoxicity, 5 which might combat cancer spread, though recent larger studies did not confirm this finding. 6 Additional studies have also shown propofol to have some inhibitory properties on cyclooxygenase and hypoxia-inducible factor 1a (HIF-1a), and to reduce cancer cell motility and invasion 7 ; all of which may minimize the activation of cancer-progression pathways. Conversely, volatile anesthetics can cause activation of insulin-like growth factors and HIF-1a.…”

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confidence: 99%

Can anesthesiologists affect cancer outcomes?

Nadler

Quinn

Bennett‐Guerrero

2019

Can J Anesth/J Can Anesth

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“…Propofol is widely used as an intravenous sedative-hypnotic agent in cancer resection surgery. 10 Besides, recent studies even found that propofol also exerts antitumor activities in several types of cancers, such as breast cancer, lung cancer, pancreatic cancer, hepatocellular carcinoma, and colon cancer. [11][12][13][14][15] Although some of the results remain controversial, overall, propofol has been considered to possesses an antitumor role on the proliferation, invasion, and metastasis of tumor cells via regulating key RNAs and signaling pathways.…”

mentioning

confidence: 99%

Effects of propofol on colon cancer metastasis through STAT3/HOTAIR axis by activating WIF‐1 and suppressing Wnt pathway

Zhang

Zhou

et al. 2020

Cancer Medicine

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Background In the present study, we aim to investigate the potential role of propofol in the tumor progression of colon cancer. Methods Human colon cancer cell lines were cultured and exposed with 8 μg/mL propofol. RNA interference was performed to silence the expression of HOTAIR or STAT3 to explore their biological functions in colon cancer. Cell apoptosis and invasion were assessed using flow cytometry and transwell assays, respectively. Quantitative real‐time PCR, western blot, and immunohistochemistry were subjected to measure the expression patterns of HOTAIR, STAT3, Wnt signaling factors, and epithelial‐mesenchymal transition‐related markers, respectively. Besides, nude mice were transplanted with colon cancer cells for further exploration. Tumor formation, volume, and weight were evaluated to validate the in vitro findings. Results Propofol treatment promoted cell apoptosis and inhibited cell invasion in colon cancer cells, while the effects were reversed by HOTAIR overexpression. Additionally, STAT3 positively regulated HOTAIR expression, which was also negatively modulated by propofol. Moreover, STAT3 and HOTAIR were shown to independently regulate colon cancer cell apoptosis and invasion. Furthermore, HOTAIR could stimulate Wnt signaling pathway via inhibiting WIF‐1 expression and upregulating β‐catenin expression, which was also demonstrated by in vivo study. Conclusion Taken together, the current study demonstrated that propofol exerts the inhibition on cell invasion and promotion on cell apoptosis through regulating STAT3/HOTAIR by activating WIF‐1 and suppressing Wnt pathway, indicating that propofol might serve as a therapeutic role for colon cancer patients in the future.

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Effects of propofol on cancer development and chemotherapy: Potential mechanisms

Cited by 89 publications

References 75 publications

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

Can anesthesiologists affect cancer outcomes?

Effects of propofol on colon cancer metastasis through STAT3/HOTAIR axis by activating WIF‐1 and suppressing Wnt pathway

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