[Corrigendum] Butein induces cell apoptosis and inhibition of cyclooxygenase­2 expression in A549 lung cancer cells.

Following the publication of the above article, the authors have realized that an error was made in the Acknowledgements section in this paper; this research was not, in fact, supported by a grant from the National Natural Science Foundation of Jilin (Project no. 83657488), as had been stated. The authors regret their oversight in providing this incorrect information in the Acknowledgements section of their paper. They thank the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this corrigendum, and apologize to the readership of the Journal for any inconvenience caused. [the original article was published in Molecular Medicine Reports 9: 763-767, 2014; DOI: 10.3892/mmr.2013.1850].

[Retracted] Downregulation of NOB1 suppresses the proliferation and tumor growth of non­small cell lung cancer in vitro and in vivo.

Oncol Rep 31: [Related article:] 1271­1276, 2014; DOI: 10.3892/or.2014.2991. The authors wish to retract their article entitled 'Down-regulation of NOB1 suppresses the proliferation and tumor growth of non­small cell lung cancer in vitro and in vivo', published in Oncology Reports 31: 1271­1276, 2014. The authors have identified that the results shown in Fig. 4A did not display a significant level of difference comparing among the groups, which undermines the conclusions stated in the article. In addition, the 'Acknowledgements' section featured an error in terms of the quoted project number. For these reasons, the authors have decided to withdraw this paper from the Journal. All the named authors agree to this retraction. and regret any inconvenience to the readers and to the Editor of Oncology Reports that this retraction will cause.

Combined cetuximab and celecoxib treatment exhibits a synergistic anticancer effect on human oral squamous cell carcinoma in vitro and in vivo.

The aim of the present study was to evaluate the potency of epidermal growth factor receptor (EGFR) pathway inhibition achieved by combining cetuximab (CET), an anti-EGFR monoclonal antibody, and celecoxib (CXB), a cyclooxygenase-2 (COX-2) inhibitor, in oral squamous cell carcinoma (OSCC) in vitro and in vivo. The OSCC cell line, HSC3, was treated with CET (0-400 µg/ml), CXB (0-40 µM), or a combination of both at a range of concentrations. Cell proliferation, apoptosis, migration and invasion were determined to assess the anticancer effects in vitro. The in vivo effects of CET and CXB on tumor cell growth were examined using an OSCC xenograft nude mouse model. In addition, downstream protein expression levels of EGFR, p-EGFR, PI3K, p-PI3K, AKT and p-Akt were evaluated by western blot analysis. It was found that the combination of low concentrations of CET and CXB significantly suppressed the proliferation, migration and invasion of the HSC3 tumor cells and decreased PEG2 production and VEGF expression in vitro, and inhibited tumor growth in vivo compared to the action of either agent alone. The results also showed that this combination significantly induced apoptosis and increased caspase-3 and caspase-8 activity compared to the action of either agent alone (P<0.01). Furthermore, the combination treatment significantly reduced the expression of p-EGFR, p-PI3K and p-Akt in the HSC3 cell line, which may contribute to the inhibition of tumor growth. Taken together, our findings revealed that the additive combination of CET and CXB is a potential drug candidate for the treatment of OSCC.

Combined cetuximab and celecoxib treatment exhibits a synergistic anticancer effect on human oral squamous cell carcinoma in vitro and in vivo.

The aim of the present study was to evaluate the potency of epidermal growth factor receptor (EGFR) pathway inhibition achieved by combining cetuximab (CET), an anti-EGFR monoclonal antibody, and celecoxib (CXB), a cyclooxygenase-2 (COX-2) inhibitor, in oral squamous cell carcinoma (OSCC) in vitro and in vivo. The OSCC cell line, HSC3, was treated with CET (0-400 µg/ml), CXB (0-40 µM), or a combination of both at a range of concentrations. Cell proliferation, apoptosis, migration and invasion were determined to assess the anticancer effects in vitro. The in vivo effects of CET and CXB on tumor cell growth were examined using an OSCC xenograft nude mouse model. In addition, downstream protein expression levels of EGFR, p-EGFR, PI3K, p-PI3K, AKT and p-Akt were evaluated by western blot analysis. It was found that the combination of low concentrations of CET and CXB significantly suppressed the proliferation, migration and invasion of the HSC3 tumor cells and decreased PEG2 production and VEGF expression in vitro, and inhibited tumor growth in vivo compared to the action of either agent alone. The results also showed that this combination significantly induced apoptosis and increased caspase-3 and caspase-8 activity compared to the action of either agent alone (P<0.01). Furthermore, the combination treatment significantly reduced the expression of p-EGFR, p-PI3K and p-Akt in the HSC3 cell line, which may contribute to the inhibition of tumor growth. Taken together, our findings revealed that the additive combination of CET and CXB is a potential drug candidate for the treatment of OSCC.

Anatomical study of insula and its relationship with the adjacent structures.

INTRODUCTION: Insular lobe is folded deep in the sylvian fissure, and the transsylvian transinsular approach is one of the most commonly used methods for lesions in the insula, basal ganglia, amygdala, and hippocampus. Hence, it is essential for surgeons to master a specific anatomic knowledge of the insula and its adjacent structures. This study aims to locate the insula, measure relevant parameters, and reduce the occurrence of surgical injury and postoperative complications. PATIENTS AND METHODS: One hundred three individuals (53 males and 50 females) were selected randomly, and magnetic resonance imaging-based morphometric analysis was performed. We located the landmark and measured the parameters related to the transsylvian transinsular approach. The parameters and figures in the sagittal, coronal, and axial planes were used to illustrate the anatomical relationship between the insular lobe and its adjacent structures. RESULTS: The length of the superior limiting sulcus (line A) was 52.05 ± 3.30 mm in the left and 51.56 ± 2.90 mm in the right. The length of the inferior limiting sulcus (line B) was 48.18 ± 3.01 mm in the left and 48.40 ± 3.34 mm in the right. The length of the anterior limiting sulcus (line C) was 22.64 ± 1.47 mm in the left and 22.50 ± 1.57 mm in the right. The length of the central insular sulcus (line D) was 31.36 ± 2.68 mm in the left and 31.52 ± 2.53 mm in the right. The distance from insular apex to brain surface through sylvian fissure (line E) was 19.26 ± 2.21 mm in the left and 19.36 ± 2.26 in the right. The distance from inferior limiting sulcus to the roof of temporal horn (line J) was 9.75 ± 1.38 mm in the left and 9.66 ± 1.18 mm in the right. The angle (θ), which was formed by line J and the vertical line via the inferior limiting sulcus (line I), was 30.51 ± 3.60 degrees in the left and 30.56 ± 3.11 degrees in the right. The distance from insular apex to the lateral side of putamen (line L) was 10.10 ± 1.59 mm in the left and 10.62 ± 1.39 mm in the right. The distance from insular apex to the middle of genu capsulae internae (line K) was 25.73 ± 1.02 mm in the left and 26.50 ± 1.15 mm in the right. Independent-samples t test showed no significant difference of the means between the right side and the left side. CONCLUSIONS: The statistics in our study can help to understand the complicated anatomical structures of insula and its surrounding area. Moreover, the parameters can increase the feasibility and safety of the surgery via transsylvian transinsular approach.

ADAM17 silencing suppresses the migration and invasion of non-small cell lung cancer.

A disintegrin and metalloprotease (ADAM) 17 has been implicated in the tumor progression of various types of solid tumor; however, little is known about its role in non-small cell lung carcinoma (NSCLC). The present study evaluated whether the downregulation of ADAM17 affects cell proliferation, the cell cycle, cell migration and cell invasion in NSCLC. A recombinant lentiviral small hairpin RNA (shRNA) expression vector carrying ADAM17 was constructed and then infected into A549 cells, a human NSCLC cell line. Cell proliferation, cell cycle progression, cell migration and cell invasion were determined following the downregulation of ADAM17 by siRNA. It was revealed that downregulation of ADAM17 expression using an RNA silencing approach in A549 tumor cells significantly suppressed cell proliferation and invasion in vitro, and tumor growth in vivo. These data suggested that ADAM17 is an important regulator of the tumorigenic properties of human NSCLC and may be used as a potential anticancer therapeutic target in NSCLC.

Downregulation of NOB1 suppresses the proliferation and tumor growth of non-small cell lung cancer in vitro and in vivo.

Non-small cell lung cancer (NSCLC) is a lethal disease due to the absence of effective diagnostic biomarkers and therapeutic targets. Therefore, novel molecular targets are critically needed to formulate new approaches for this devastating disease. In the present study, using quantitive real-time PCR and immunohistochemistry. we initially found that expression of the ribosome assembly factor NIN/RPN12 binding protein (NOB1) was elevated in the majority of NSCLC tissues when compared to that in the normal lung tissue counterparts, and its expression level was correlated with key pathological characteristics including tumor differentiation, stage and metastasis. Then, the recombinant lentiviral shRNA expression vector carrying NOB1 was constructed and infected into the human NSCLC A549 cell line. Cell proliferation, cell apoptosis, cell cycle distribution and colony formation ability in A549 cells were assessed following downregulation of NOB1 by siRNA. In addition, tumor growth ability in nude mice was evaluated to define the function of NOB1 in cell transformation and tumorigenesis. It was found that downregulation of NOB1 expression using the RNA silencing approach in A549 tumor cells significantly suppressed the proliferation and colony formation ability, and induced tumor apoptosis in vitro. Tumor growth was also suppressed in vivo. These data suggest that NOB1 is an important regulator of the tumorigenic properties of human NSCLC and may be used as a new promising diagnostic biomarker and a potential anticancer therapeutic target for NSCLC.

Butein induces cell apoptosis and inhibition of cyclooxygenase­2 expression in A549 lung cancer cells.

Butein is a flavonoid isolated from the bark of Rhus verniciflua Stokes and the flowers of Butea monosperma, and is known to be a potential therapeutic drug for treating inflammation and cancer. Cyclooxygenase (COX) converts arachidonic acid to prostanoids, and increased expression of its isoform, COX­2, has been observed in lung cancer tissue. The aim of the present study was to investigate expression alteration of COX­2 in A549 lung cancer cells following butein treatment at the mRNA and protein levels by quantitative polymerase chain reaction and western blotting, respectively. It was observed that COX­2 mRNA and protein levels were significantly downregulated in the butein treatment group in comparison with the control group (P<0.05). In addition, the effects of butein on proliferation and apoptosis were evaluated. The data demonstrated that butein induces cell­cycle arrest and apoptosis in human lung cancer cells. These results indicated that butein may be a promising candidate drug for lung cancer treatment.