Effects of propofol on the development of cancer in humans

Abstract

Cancer is one of most the significant threats to human health worldwide, and the primary method of treating solid tumours is surgery. Propofol, one of the most widely used intravenous anaesthetics in surgery, was found to be involved in many cancer-related pathophysiology processes, mainly including anti-tumour and minor cancer-promoting effects in various types of cancer. An increasing number of studies have identified that propofol plays a role in cancer by regulating the expression of multiple signalling pathways, downstream molecules, microRNAs and long non-coding RNAs. Emerging evidence has indicated that propofol can enhance the anti-tumour effect of chemotherapeutic drugs or some small molecular compounds. Additionally, in vivo animal models have shown that propofol inhibits tumour growth and metastasis. Furthermore, most clinical trials indicate that propofol is associated with better survival outcomes in cancer patients after surgery. Propofol use is encouraged in cancers that appear to have a better prognosis after its use during surgery. We hope that future large and prospective multicenter studies will provide more precise answers to guide the choice of anaesthetics during cancer surgery.

Keywords: cancer; miRNAs; prognosis; propofol; signalling pathways.

FIGURE 1

Propofol exerts tumour‐suppressive or oncogenic effects by regulation of related signalling pathways or downstream molecules in cancer cells. Akt, protein kinase B; Bax, B‐cell lymphoma‐2 associated X; Bcl‐2, B‐cell lymphoma‐2; CAMKII, calcium/calmodulin‐dependent protein kinase II; ERK, extracellular signal‐regulated kinases; FoxO1, Forkhead Box O1; ING3, inhibitor of growth 3; MAPK, mitogen‐activated protein kinase; MMP, matrix metalloproteinase; mTOR, mammalian target of rapamycin; NF‐κB, nuclear factor‐kappa B; NMDAR, N‐methyl‐D‐aspartate receptor; Nrf2, nuclear factor E2‐related factor‐2; p53, tumour protein P53; p70S6K, p70 ribosomal protein S6 kinase; Sox4, SRY‐box transcription factor 4; Wnt, wingless and proto‐oncogene integration‐1. “Arrows from propofol to → targets” means “activating targets.” “Blockade from propofol to targets” means “inhibiting targets”

FIGURE 2

The anti‐tumour effect of propofol by upregulation of miRNAs in cancer cells. AKT, protein kinase B; Bcl‐2, B‐cell lymphoma‐2; JAK, Janus kinase; miR, microRNAs; MMP, matrix metalloproteinase; NF‐κB, nuclear factor‐kappa B; STAT, signal transducer and activator of transcription 3; Wnt, wingless and proto‐oncogene integration‐1. “Arrows from propofol to → targets” means “activating targets.” “Blockade from propofol to targets” means “inhibiting targets”

FIGURE 3

The anti‐tumour effect of propofol by downregulation of miRNAs or lncRNAs in cancer cells. AKT, protein kinase B; ATG5, autophagy‐related genes 5; HOTAIR, HOX antisense intergenic RNA; HOXA11‐AS, HOXA11 Antisense RNA; MALAT1, metastasis‐associated lung adenocarcinoma transcript 1; miR, microRNAs; mTOR, mammalian target of rapamycin; p27, cyclin‐dependent kinase inhibitor 1B; PI3K, phosphoinositide 3‐kinase; RAC1, Ras‐related C3 botulinum toxin substrate 1; Wnt, wingless and proto‐oncogene integration‐1. “Arrows from propofol to → targets” means “activating targets.” “Blockade from propofol to targets” means “inhibiting targets”