Search

Standard chemotherapy is commonly used in clinical practice for the treatment of non-small cell lung cancer (NSCLC). However, its therapeutic efficacy remains low. Combination therapy for cancer treatment has attracted attention in recent years. The present study aimed to investigate the antitumor effect of the combination treatment with gemcitabine and sorafenib on NSCLC in vitro and in vivo, and to determine its underlying molecular mechanisms. The anti-NSCLC effects of combination therapy were analyzed by flow cytometry analysis, MTT, western blotting, reverse transcription-quantitative PCR, wound healing and Transwell invasion assays. A549 cells subjected to combination treatment with gemcitabine and sorafenib demonstrated a more irregular cellular morphology and lower cell viability compared with the monotherapy groups. Combination of gemcitabine and sorafenib significantly induced cell cycle arrest and apoptosis in A549 cells. Additionally, combination therapy was demonstrated to restrain the migration and invasion of tumor cells by suppressing epithelial-to-mesenchymal transition (EMT) of A549 cells. In vivo analyses confirmed that co-treatment with gemcitabine and sorafenib decreased NSCLC tumor growth and tumor weight in nude mice. Taken together, the results of the present study suggested that combination treatment with gemcitabine and sorafenib exerted a synergistic inhibitory effect on NSCLC in vitro and in vivo via the EMT process. [ABSTRACT FROM AUTHOR]

(B) Agarose gel electrophoresis (1.2%) exhibited a single and specific polymerase chain reaction product of each reference gene. Oncol Lett 14: 6001-6011, 2017; DOI: 10.3892/ol.2017.7002 Following the publication of the above article, the authors have realized that they inadvertently included the same data for the HSP90AB1 and ATP5B experiments shown in Fig. [Extracted from the article]

Breast cancer is a highly heterogeneous disease at the molecular level and >90% of mortalities are due to metastasis and its associated complications. The present study determined the impact of molecular subtypes on metastatic behavior and overall survival (OS) of patients with metastatic breast cancer. The influence of molecular subtypes on the sites and number of metastases in 166 patients with metastatic breast cancer from a single center were assessed; and the influence of molecular subtypes on the sites and number of metastases and OS in 15,322 metastatic cases among 329,770 patients with primary breast cancer from the Surveillance, Epidemiology and End Results database were assessed. Analysis of both datasets revealed that different molecular subtypes exhibited differences in the prevalence of different metastatic sites and number of metastases. A larger proportion of bone metastasis was observed in the hormone receptor (HR)+/human epidermal growth factor receptor 2 (HER2)+ subtype than in other subtypes, more lung metastasis was observed in the HR-/HER2+ subtype and more liver metastasis occurred in the HR+/HER2+ and HR-/HER2+ subtypes. Single-site metastasis was more common for the HR+/HER2− subtype than in other subtypes, while 2–3 sites of metastases were more common for the HR+/HER2+ subtype and ≥4 sites of metastases were more frequent in the HR-/HER2+ and HR-/HER2- subtypes. The mean OS of patients with primary breast cancer in the HR+/HER2− subtype group was the longest (78.5 months), while the HR-/HER2- group had the shortest mean OS (69.1 months). The mean OS of the metastatic HR+/HER2+ group was the longest (46.0 months), while the mean OS of the metastatic HR-/HER2- group was the shortest (18.5 months). In conclusion, the results of the present study suggested that different molecular subtypes of breast cancer have different metastatic behavior, as well as mean OS. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the effect of 5-aza-2'-deoxycytidine (decitabine; DAC) and all- trans retinoic acid (ATRA) on Wilms' tumor 1 (WT1) in acute myeloid leukemia (AML) in vitro . The methylation status of the WT1 promoter was analyzed using methylation-specific polymerase chain reaction (MSP). The expression level of WT1 was detected by reverse transcription-quantitative polymerase chain reaction. The effect of DAC and ATRA on cell differentiation was evaluated by flow cytometry. The WT1 gene was methylated in U937 cells, but unmethylated in SHI-1 and K562 cells; the U937 cells did not express the WT1 gene, but the SHI-1 and K562 cells highly expressed the WT1 gene. DAC and ATRA, alone or in combination, exhibited no effect on the expression level of WT1 in the U937 cells and on the differentiation of the K562 cells. The combined treatment of DAC and ATRA markedly decreased the WT1 expression levels of the SHI-1 and K562 cells, and induced the differentiation of the SHI-1 and U937 cells. In the SHI-1 cells, WT1 expression changed inversely to the dynamic changes of cluster of differentiation 11b-positive rates. In conclusion, the combined treatment of DAC and ATRA has clinical therapeutic potential in acute monocytic leukemia patients with high WT1 expression and a poor response to standard induction chemotherapy.