Author Correction: Propofol inhibits invasion and enhances paclitaxel-induced apoptosis in ovarian cancer cells through the suppression of the transcription factor slug.

Correction to: European Review for Medical and Pharmacological Sciences 2013; 17 (13): 1722-1729-PMID: 23852894, published online on 15 July 2013. The authors found some mistakes in the article. • The band of ß-actin in Figure 2 was an inadvertent wrong use due to an error in figure preparation. The authors confirm that the correction does not affect the discussion and conclusions of the original article. There are amendments to this paper. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/4537.

Effect of downregulated lncRNA NBAT1 on the biological behavior of glioblastoma cells.

OBJECTIVE: To investigate the expression of lncRNA neuroblastoma associated transcript 1 (NBAT1) in human glioma cell lines and its underlying mechanism. Effect of NBAT1 on biological behaviors of T98 and U87 cells are also explored. PATIENTS AND METHODS: The mRNA expressions of NBAT1 in 48 cases of glioblastoma tissues and 30 cases of normal brain tissues were accessed by Real-time fluorescence quantitative PCR (RT-PCR). The relationship between mRNA expression of NBAT1 and tumor size, malignancy, and prognosis were analyzed. Effects of NBAT1 on the proliferation of glioblastoma T98 and U87 cells were determined by CCK-8 assay and colony formation assay, respectively. RESULTS: NBAT1 expressions in glioblastoma tissues were lower than those in normal brain tissues, which was negatively correlated with malignancy degree (p<0.01). Protein levels of Akt were decreased in T98 and U87 cells transfected with si-NBAT1. Meanwhile, proliferation abilities of T98 and U87 cells transfected with si-NBAT1 were significantly decreased as well (p<0.01), which were reversed by transfection of si-Akt. CONCLUSIONS: Upregulated NBAT1 inhibits proliferation of T98 and U87 cells via regulating Akt, indicating that NBAT1 may be related to the malignancy and prognosis of gliomas.

Propofol suppresses invasion and induces apoptosis of osteosarcoma cell in vitro via downregulation of TGF-ß1 expression.

OBJECTIVE: Osteosarcoma (OS) is the most common malignant tumor of the bone, with a high mortality rate and poor prognosis. Propofol has been proposed to play a role of antitumor in various cancers. However, the functions and mechanisms of propofol in OS is still not clear. MATERIALS AND METHODS: The different concentrations of propofol were co-incubated with osteosarcoma MG-63 lines for 72 hrs. Cell proliferation, apoptosis, and invasion were detected by MTT assay, Flow cytometry analysis, and Matrigel invasion assay. Western blot was used to detect the TGF-ß1 protein levels. MG-63 cells were treated with human recombinant TGF-ß1 (rh TGF-ß1) to assess the role of TGF-ß1 in propofol-induced anti-tumor activity. RESULTS: Propofol significantly inhibited cell proliferation and invasion and promoted apoptosis of MG-63 lines cells. Propofol also efficiently reduced TGF-ß1 expression. Moreover, restoration of TGF-ß1 by rhTGF-ß1 treatment reversed the effects of propofol on the biological behavior of OS cells. CONCLUSIONS: Propofol can effectively inhibit proliferation and invasion and induce apoptosis of OS cells through, at least partly, downregulation of TGF-ß1 expression.

Propofol suppresses proliferation, invasion and angiogenesis by down-regulating ERK-VEGF/MMP-9 signaling in Eca-109 esophageal squamous cell carcinoma cells.

BACKGROUND AND AIMS: Propofol (2,6-diisopropylphenol), one of the most commonly used intravenous anaesthetic agents during cancer resection surgery, has been reported to have the ability of influencing the invasion of human cancer cells. However, the mechanisms are not very clear. In this study, we investigated the effects of propofol on the proliferation, invasion and angiogenesis of human Eca-109 cells, and explored the mechanism. METHODS: The human Eca-109 cells was treated with propofol at the concentrations of 10-100 µmol/L for 72 hours or at the concentration of 100 µmol for 8-72 hours. Cell viability was determined by the MTT assay; the effect of propofol on apoptosis by 5'-triphosphate-biotin nick end labeling (TUNEL) staining. The effect of propofol on angiogenesis was determined by the chicken chorioallantoic membrane (CAM) angiogenesis assay. The effect of propofol on cell invasion using a modified Matrigel Boyden chamber assay. ERK1/2, MMP-9 and VEGF leves was detected by western blotting assay. RESULTS: In human Eca-109 cells, propofol significantly promoted cell apoptosis and inhibited proliferation in a dose and time-dependent manner. Furthermore, propofol inhibited dose and time-dependent invasion and angiogenesis. Propofol significantly dose and time-dependently down-regulated gene expression and protein production of ERK/pERK, VEGF and MMP-9. The functional effects and MMP-9/VEGF inhibition were shown to be dependent on the ERK/VEGF and ERK/MMP-9 signaling pathways. It was noteworthy that the ERK activator (phorbol 12-myristate 13-acetate [PMA]) treatment increased the MMP-9/VEGF levels after propofol treatment, and led to significant increase of proliferation, invasion and angiogenesis. CONCLUSIONS: These findings indicate that propofol inhibited proliferation, invasion and angiogenesis of human Eca-109 cells in vitro through modulation of ERK-VEGF /MMP-9 signaling. Propofol not only can be an anesthesia agent which reduces pain but plays an important role of inhibiting the migration and angiogenesis of ESCC cells in the therapy of ESCC patients.

Propofol inhibits invasion and enhances paclitaxel- induced apoptosis in ovarian cancer cells through the suppression of the transcription factor slug.

BACKGROUND AND AIM: Propofol is one of the most commonly used intravenous anaesthetic agents during cancer resection surgery. It has recently found that propofol has the effect to inhibit cancer cell migration and invasion and sensitize cancer cells to chemotherapy. However, the role of the propofol on the ovarian cancer cells is unknown. In the present study, we explored the effect of propofol on invasion and chemosensitization of ovarian cancer cells to paclitaxel. MATERIALS AND METHODS: The paclitaxel sensitivity of ovarian cancer cell lines HO-8910PM, H0-8910, SKOV-3, OVCAR-3, COC1 and ES-2 were determined by MTT assays. The Slug levels in the cell lines and the effects of propofol on Slug levels in the cell lines were determined by western blot assays. The effect of propofol on invasion, migration and paclitaxel-induced ovarian cancer apoptosis was determined by Boyden chamber assays, cell MTT, TUNEL assays. RESULTS: The results showed that the cell lines COC1, H0-8910 and ES-2 were sensitive, whereas HO-8910PM, OVCAR-3, SKOV-3, were resistant to paclitaxel. Significant correlation was observed between basal Slug levels and paclitaxel sensitivity. Paclitaxel treatment increased Slug levels. Treatment with propofol induced apoptosis and increased paclitaxel killing of all paclitaxel-sensitive and -resistant ovarian cancer cells followed by significant decrease in the Slug levels. Treatment with propofol inhibits invasion and migration. CONCLUSIONS: These data suggest a new mechanism by which the propofol inhibits invasion and metastasis,enhances paclitaxel-induced ovarian cancer cell apoptosis through suppression of Slug.