[Retracted] Bergamottin isolated from Citrus bergamia exerts in vitro and in vivo antitumor activity in lung adenocarcinoma through the induction of apoptosis, cell cycle arrest, mitochondrial membrane potential loss and inhibition of cell migration and invasion.

Following the publication of the above paper, a concerned reader drew to the Editor's attention that a number of figures (specifically, Figs. 6, 8, 9, 10 and 12) contained apparent anomalies, including repeated patternings of data within the same figure panels. After having conducted an independent investigation in the Editorial Office, the Editor of Oncology Reports has determined that this paper should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office never received any reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [the original article was published in Oncology Reports 36: 324­332, 2016; DOI: 10.3892/or.2016.4833].

Bergamottin isolated from Citrus bergamia exerts in vitro and in vivo antitumor activity in lung adenocarcinoma through the induction of apoptosis, cell cycle arrest, mitochondrial membrane potential loss and inhibition of cell migration and invasion.

The objective of the present study was to investigate the in vitro and in vivo anticancer properties of bergamottin, a natural furanocoumarin, against human non-small cell lung carcinoma (NSCLC) A549 cells. We also studied its effect on cell proliferation, cell cycle arrest, cell invasion, cell migration as well as cell apoptosis. Antiproliferative activity of bergamottin was estimated by the MTT assay. Phase contrast and fluorescence microscopy as well as flow cytometry using Annexin V-FITC assay were used to study induction of apoptosis by bergamottin in these cells. The effects of bergamottin on cell cycle phase distribution as well as on mitochondrial membrane potential were also demonstrated using flow cytometry. In vitro wound healing assay was used to study the effect of bergamottin on cell migration. The effects of bergamottin on tumor progression were also observed using a nude mouse model. The mice were divided into 4 groups and treated with bergamottin injected intraperitoneally. Bergamottin induced dose-dependent as well as time-dependent cytotoxic effects as well as inhibition of colony formation in the A549 cancer cells. Bergamottin also suppressed cancer cell invasion as well as cancer cell migration. Phase contrast microscopy and fluorescence microscopy revealed that bergamottin induced cell shrinkage, chromatin condensation and the cells became rounded and detached from each other. Bergamottin also induced a potent cell cycle arrest at the G2/M phase of the cell cycle. Experiments in mice showed that 25, 50 and 100 mg/kg bergamottin injection reduced the tumor weight from 1.61 g in the phosphate-buffered saline (PBS)-treated group (control) to 1.21, 0.42 and 0.15 g in the bergamottin-treated groups, respectively. The results of the present study revealed that bergamottin was able to inhibit lung cancer cell growth both in a cell model and a xenograft mouse model by inducing apoptosis, mitochondrial membrane potential loss, G2/M cell cycle arrest as well as inhibiting cell migration and invasion.

Positive association between miR-499A>G and hepatocellular carcinoma risk in a Chinese population.

A case-control study of the association of miR-499A>G rs3746444 with risk of hepatocellular carcinoma (HCC)was conducted. Patients with HCC and healthy control subjects were recruited for genotyping of miR- 499A>G using duplex polymerase-chain-reaction with confronting-two-pair primer(PCR-RFLP) analysis. The MiR-499 GG genotype was associated with a decreased risk of HCC as compared with the miR-499 AA genotype (adjusted OR=0.74, 95%CI=0.24-0.96). Similarly, the GG genotype showed a 0.45-fold decreased HCC risk in a recessive model. The MiR-499 G allele was significantly associated with decreased risk of HCC among patients infected with HBV in a dominant model (OR=0.09, 95%CI= 0.02-0.29). In conclusion, the MiR-499A>G rs3746444 polymorphism is associated with HCC risk in the Chinese population, and may be useful predictive marker for CAD susceptibility.

Prediction role of seven SNPs of DNA repair genes for survival of gastric cancer patients receiving chemotherapy.

We aimed to investigate DNA repair gene expression of response to chemotherapy among gastric patients, and roles in the prognosis of gastric cancer. A total of 209 gastric cancer patients were included in this study between January 2007 and December 2008, all treated with chemotherapy. Polymorphisms were detected by real time PCR with TaqMan probes, and genomic DNA was extracted from peripheral blood samples. The overall response rate was 61.2%. The median progression and overall survivals were 8.5 and 18.7 months, respectively. A significant increased treatment response was found among patients with XPG C/T+T/T or XRCC1 399G/ A+A/A genotypes, with the OR (95% CI) of 2.14 (1.15-4.01) and 1.75 (1.04-3.35) respectively. We found XPG C/T+T/T and XRCC1 399 G/A+A/A were associated with a longer survival among gastric cancer patients when compared with their wide type genotypes, with HRs and 95% CIs of 0.49 (0.27-0.89) and 0.56 (0.29-0.98) respectively. Selecting specific chemotherapy based on pretreatment genotyping may be an innovative strategy for further studies.

[Abnormal expression of hMSH2 mRNA and mutation P53 protein in acute lymphoblastic leukemia].

In order to investigate the mechanism of acute lymphoblastic leukemic cell malignant proliferation, the expressions of hMSH2 mRNA and mutation P53 (mtP53) protein in bone marrow cells of de novo acute lymphoblastic leukemia (ALL) were determined by in situ hybridization and immunocytochemical methods. The results showed the that percentage of positive cell with hMSH2 mRNA expression was (32.88 +/- 11.46)% in the de novo ALL group and (64.22 +/- 8.51)% in the control group. The percentage of positive cell with mtP53 protein expression was (29.25 +/- 9.45)% in the de novo ALL group, and (12.63 +/- 6.66)% in the control group. There was a significant negative correlation between the positive percentages of hMSH2 mRNA expression and mtP53 protein expression (r = -0.45, P < 0.05). It is concluded that defective MSH2 mRNA expression plays an important role in the pathogenesis of acute lymphoblastic leukemia, mtP53 protein mutation plays an important role in the development of acute lymphoblastic leukemia, the hMSH2 mRNA defect can lead to accumulation of the mutant P53 protein in acute lymphoblastic leukemia, and both jointly promote the pathogenesis of ALL.

Detection of aberrant p16 methylation in the serum of colorectal cancer patients.

PURPOSE: This study was designed to detect aberrant p16 promoter methylation in the serum of patients with colorectal cancer (CRC) and to explore the possibility of using this assay in early detection or as a prognostic marker of CRC patients. EXPERIMENTAL DESIGN: Methylation-specific PCR was used to detect p16 methylation in DNA extracted from 52 CRCs and matching serum samples and control serum samples from 34 patients with adenomatous polyps and 10 healthy individuals. The association of p16 hypermethylation in serum DNA of CRC patients with clinicopathological characteristics was then analyzed. RESULTS: P16 hypermethylation was found in 20 of 52 (38%) CRCs. Among the 20 cases with aberrant methylation in the tumor tissues, similar changes were also detected in the serum of 14 (70%) cases. No methylated p16 sequences were detected in the peripheral serum of the other 32 CRC cases without these changes in the tumor, in 34 patients with adenomatous polyps, or in 10 healthy control subjects. Clinicopathological analysis revealed that p16 methylation in serum was significantly associated with later Dukes' stage (P = 0.03). CONCLUSIONS: This assay offers a potential means for the serum-based detection and/or monitoring of CRC patients.