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 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, COX‑2, has been observed in lung cancer tissue. The aim of the present study was to investigate expression alteration of COX‑2 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 COX‑2 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 cell‑cycle arrest and apoptosis in human lung cancer cells. These results indicated that butein may be a promising candidate drug for lung cancer treatment.
Abstract. 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. IntroductionOral squamous cell carcinoma (OSCC) accounts for approximately 4% of all carcinomas in men and 2% in women worldwide, with geographical variation in frequency (1). Although advances in early diagnosis and multimodal treatments, including surgery, chemotherapy and irradiation have been achieved, the 5-year survival rate of OSCC patients has remained at 50-60% due to recurrence and metastasis (2). Since conventional cytotoxic therapies act upon rapidly dividing normal cells as well as malignant cells, which results in the significant morbidity in patients with solid tumors including OSCC, this method is of limited benefit for survival (3). Therefore, the development of improved anticancer therapies that effectively and specifically target epithelial tumor cells while minimizing the toxic side effects commonly associated with conventional cytotoxic therapies is urgently needed.With the enhanced understanding of key cellular pathways involved in tumor growth, progression and cell death, molecular targeted therapies have been exploited (4). Recently, novel treatments aimed to target specific molecules, such as epidermal growth factor receptor (EGFR), aberrantly expressed in OSCC, have been investigated and tested in clinical trials at several research centers with promising results (5). For many years, the EGFR has been investigated as a major target for the treatment of uncontrolled tumor growth (6). The EGFR, a gl...
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.
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.
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