Breast cancer is the second leading cause of cancer death in women. Surgery is the first line of treatment for breast cancer. Retrospective clinical studies suggest that the type of anesthesia administered during oncological surgery may influence patient outcome. Propofol, the widely used intravenous anesthetic agent, may lead to better outcomes compared to volatile anesthetics. Here we review the literature on the effect of propofol in breast cancer cells, the immune system, pain management, and patient outcomes. Evidence from the study of breast cancer cell lines suggests that high concentrations of propofol have both anti-tumor and pro-tumor effects. Propofol and volatile anesthetics have different effects on the immune system. Propofol has also been shown to reduce the development and severity of acute and chronic pain following surgery. Although a retrospective study that included many types of cancer indicated that propofol increases the long-term survival of patients following surgery, the evidence for this in breast cancer is weak. It has been shown that Propofol combined with paravertebral block led to change of serum composition that affects the breast cancer cell behaviors and natural killer cell activity. Prospective studies are in progress and will be finished within 5 years. The existing evidence is not sufficient to warrant changes to current anesthetic management. Further research is needed to clarify the mechanisms by which propofol affects cancer cells and the immune system.

/pdf/effect-of-propofol-on-breast-cancer-cell-the-immune-system-fjbmflymw2.pdf

Effect of Propofol on breast Cancer cell, the immune system, and patient outcome

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

Effects of propofol on the development of cancer in humans

MOTIVATION Disease is often manifested via changes in transcript and protein abundance. MicroRNAs (miRNAs) are instrumental in regulating protein abundance and may measurably influence transcript levels. miRNAs often target more than one mRNA (for humans, the average is three), and mRNAs are often targeted by more than one miRNA (for the genes considered in this study, the average is also three). Therefore, it is difficult to determine the miRNAs that may cause the observed differential gene expression. We present a novel approach, maTE, which is based on machine learning, that integrates information about miRNA target genes with gene expression data. maTE depends on the availability of a sufficient amount of patient and control samples. The samples are used to train classifiers to accurately classify the samples on a per miRNA basis. Multiple high scoring miRNAs are used to build a final classifier to improve separation. RESULTS The aim of the study is to find a set of miRNAs causing the regulation of their target genes that best explains the difference between groups (e.g. cancer versus control). maTE provides a list of significant groups of genes where each group is targeted by a specific miRNA. For the datasets used in this study, maTE generally achieves an accuracy well above 80%. Also, the results show that when the accuracy is much lower (e.g. ∼50%), the set of miRNAs provided is likely not causative of the difference in expression. This new approach of integrating miRNA regulation with expression data yields powerful results and is independent of external labels and training data. Thereby, this approach allows new avenues for exploring miRNA regulation and may enable the development of miRNA-based biomarkers and drugs. AVAILABILITY AND IMPLEMENTATION The KNIME workflow, implementing maTE, is available at Bioinformatics online. SUPPLEMENTARY INFORMATION Supplementary data are available at Bioinformatics online.

maTE: discovering expressed interactions between microRNAs and their targets.

The involvement of propofol and circular RNAs (circRNAs) in lung cancer progression has been identified. However, the relationship between propofol and circRNAs as well as the underlying molecular mechanisms on lung cancer development remain unclear. Cell viability, migration and invasion were measured by cell counting kit-8 assay, 5-bromo-2-deoxyuridine (BrdU) and transwell assay. Glycolytic metabolism was calculated by measuring the glucose consumption, lactate production and extracellular acidification. Western blot was used to detect the protein of glucose transporter 1 (GLUT1), glycolysis enzymes, and forkhead box M1 (FOXM1). The expression of circRNA transcriptional adaptor 2A (circTADA2A), microRNA (miR)-455-3p and FOXM1 mRNA was detected by quantitative real-time polymerase chain reaction. The interaction between miR-455-3p and circTADA2A or FOXM1 was analyzed using the dual-luciferase reporter assay. Murine xenograft model was established to perform in vivo experiments. We found propofol treatment alleviated lung cancer cell proliferation, migration, invasion and aerobic glycolysis in vitro as well as inhibited tumor growth in vivo. Propofol decreased the level of circTADA2A and exerted anti-tumor effects by regulating circTADA2A. MiR-455-3p directly interacted with circTADA2A and FOXM1 in lung cancer cells, and circTADA2A could regulate FOXM1 expression by binding to miR-455-3p. Subsequently, rescue assay showed that propofol inhibited cell proliferation, migration, invasion and aerobic glycolysis by regulating circTADA2A/miR-455-3p/FOXM1 axis in lung cancer. Collectively, propofol suppressed cell carcinogenesis and aerobic glycolysis by regulating circTADA2A/miR-455-3p/FOXM1 axis in lung cancer, providing an effective clinical implication for propofol to prevent the development of lung cancer.

Propofol disrupts cell carcinogenesis and aerobic glycolysis by regulating circTADA2A/miR-455-3p/FOXM1 axis in lung cancer

Propofol, a common intravenous anesthetic, has been found to exert anti-cancer effects with inhibition of cancer cell proliferation, migration and invasion. We tested its possible action against HER2-overexpressing breast cancer cells that developed resistance against trastuzumab. Cell viability assay, ELISA for cytokines, mammosphere formation, quantitative RT-PCR for EMT/IL-6-targeting miRNAs and the in vivo experimental pulmonary metastasis model were performed to understand the epigenetic action of propofol. Propofol sensitized HER2 overexpressing cells to trastuzumab but such action was even more pronounced in resistant cells. Increased cytokines IL-6 as well as IL-8 were released by resistant cells, along with increased mammospheres and induction of EMT, all of which was inhibited by propofol. IL-6 targeting tumor suppressor miR-149-5p was found to be the novel miRNA that was up-regulated by propofol, resulting in the observed effects on cell viability, IL-6 production, mammospheres generation as well as EMT induction. Further, antagonizing miR-149-5p attenuated the propofol effects confirming the epigenetic activity of propofol through miR-149-5p regulation. Finally, in vivo validation in an experimental metastasis model conformed an inhibitory action of propofol against experimental lung metastasis and the essential mechanistic role of miR-149-5p/IL-6 loop. These results present a novel role of general anesthetic propofol against resistant breast cancer cells and the underlying epigenetic regulation of a tumor suppressor miRNA.

/pdf/anesthetic-propofol-epigenetically-regulates-breast-cancer-2feyswxdo5.pdf

Anesthetic propofol epigenetically regulates breast cancer trastuzumab resistance through IL-6/miR-149-5p axis

Background and objective Propofol, an intravenous anesthetic agent, has been found to inhibit growth of breast cancer cells. However, the mechanisms underlying the antitumor are not known. A recent report has found that propofol could significantly downregulate miR-24 expression in the human malignant cancers. In breast cancer cells, overexpression of miR-24 promotes cell proliferation and inhibits cell apoptosis by downregulation of p27. The miR-24 has been reported to be overexpressed in breast cancer and breast cancer cell lines. In the present study, we hypothesized that propofol induces apoptosis of breast cancer cells by miR-24/p27 signal pathway. Methods Breast cancer MDA-MB-435 cells were exposed to propofol (10 μM) for 6 hr and cell death was assessed using TUNEL staining, Flow cytometry and cleaved caspase-3 expression. microRNA-24 (miR-24) expression was assessed using quantitative reverse transcription polymerase chain reaction (qRT-PCR). miR-24 was overexpressed using a miR-24 mimic. P27 was knocked down using a small interfering RNA. p27 and cleaved caspase-3 expression was assessed by Western blot. Results MDA-MB-435 exposed to propofol showed a significant increase in apoptotic cells, followed by the downregulation of miR-24, upregulation of p27 expression and cleaved caspase-3 expression. Targeting p27 inhibits propofol-induced cell apoptosis; miR-24 overexpression decreased propofol-induced cell apoptosis, cleaved caspase-3 and p27 expression. Conclusions Propofol inducescell death in MDA-MB-435 cells via inactivation of miR-24/p27 signal pathway.

Propofol induces apoptosis of breast cancer cells by downregulation of miR-24 signal pathway.

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Xia Miao

Author Tools

Chat about Author

Papers

Propofol induces apoptosis of breast cancer cells by downregulation of miR-24 signal pathway.