Furthermore, ARL2 overexpression decreased proliferation and weakened the colony-formation abilities of the CRC cells, as well as their migratory and invasive abilities. ARL2 interference enhanced proliferation and colony-formation rates of the CRC cells, as well as their migratory and invasive abilities. ARL2 regulated CRC proliferation and tumorigenicity and was negatively associated with AXL. The results of the present study suggested that the proliferation, migration and tumorigenicity of the CRC cells could be inhibited by ARL2 overexpression. The latter may be used as a predicted and potential therapeutic target for CRC.[This corrects the article DOI 10.3892/ol.2015.3769.].In recent years, among all patients with colorectal cancer, the proportion of young patients has been gradually increasing. However, the molecular mechanisms involved in colorectal cancer in the young are largely unknown. In the present study the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas datasets were integrated to elucidate the key gene biomarkers in these patients. The GSE41657 and GSE41258 datasets were downloaded from the GEO database. By screening for differentially expressed genes, Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes pathway analysis, protein-protein interaction analysis, hub gene screening and survival analysis, two key genes, CXCL8 and VEGFA, which were enriched in cancer pathways, were obtained. Reverse transcription-quantitative (RT-q)PCR was performed to verify the outcome obtained by bioinformatics analysis. In conclusion, the present study identified two key genes using bioinformatics analysis and RT-qPCR validation. These results indicated that the candidate genes may be involved in the progression of colorectal cancer in young people, and these two genes may act as ideal prognostic indicators or therapeutic targets for colorectal cancer in the youth.Colorectal cancer (CRC) is a common digestive system malignancy and a major cause of cancer-associated mortality worldwide. Aberrant expression of long non-coding RNAs has been reported in several types of cancer. The aim of the present study was to investigate the role of ovarian tumor domain containing 6B antisense RNA1 (OTUD6B-AS1) in CRC and its underlying mechanisms. OTUD6B-AS1 expression in CRC cell lines was examined using reverse transcription-quantitative PCR. Furthermore, The Cancer Genome Atlas database was utilized to examine the expression levels of OTUD6B-AS1 in CRC tissues. Following OTUD6B-AS1 overexpression, Cell Counting Kit-8 and colony formation assays were used to detect the proliferation ability of HCT116 cells. The expression levels of proliferation-related protein Ki67 were determined using immunofluorescence staining. Subsequently, Transwell and wound healing assays were used to evaluate the invasion and migration of HCT116 cells, respectively. The expression levels of migration-relatRC treatment.Flavonoids, a subclass of polyphenols, have been shown to be effective against several types of cancer, by decreasing proliferation and inducing apoptosis. Therefore, the aim of the present study was to assess the anti-carcinogenic potential of luteolin on HeLa human cervical cancer cells, through the use of a cell viability assay, DNA fragmentation assay, mitochondrial membrane potential assay, cell cycle analysis using Annexin/PI staining and flow cytometry, gene expression analysis and a protein profiling array. Luteolin treatment exhibited cytotoxicity towards HeLa cells in a dose- and time-dependent manner, and its anti-proliferative properties were confirmed by accumulation of luteolin-treated cells in sub-G1 phases. Cytotoxicity induced by luteolin treatment resulted in apoptosis, which was mediated through depolarization of the mitochondrial membrane potential and DNA fragmentation. Furthermore, luteolin treatment increased the expression of various proapoptotic genes, including APAF1, BAX, BAD, BID, luteolin in a dose-dependent manner, indicating its anti-proliferative and apoptosis enabling properties, and this may have been mediated via inhibition of the AKT and the MAPK pathways.CD90, also known as Thy-1 cell surface antigen, is located on human chromosome 11q23.3, and encodes a glycosylphosphatidylinositol-linked cell surface glycoprotein. CD90 serves a key role in malignancy by regulating cell proliferation, metastasis and angiogenesis. Gastric cancer is one of the most common types of malignancy. Patients with advanced gastric cancer have a poor prognosis. CD90 plays a key role in the occurrence and progression of gastric cancer.  https://www.selleckchem.com/products/Nolvadex.html  However, the molecular mechanism of CD90 in gastric cancer is currently unclear. In order to identify the molecular mechanism by which CD90 affects the biological behavior and energy metabolism of gastric cancer cells, the present study used Cell Counting Kit-8 assays, lactate concentration determination and ATP content determination. The results demonstrated that CD90 promotes proliferation and inhibits senescence in gastric cancer cells. In addition, CD90 enhanced the invasion and migration abilities of AGS gastric cancer cells. Overexpression of CD90 resulted in the accumulation of intracellular lactic acid in AGS cells. CD90 upregulated lactate dehydrogenase levels and increased the NADPH/NADP+ ratio in AGS cells. CD90 overexpression decreased the ATP concentration in AGS cells. PI3K, PDK1, phosphorylated-AKT-Ser473, HIF-1α, MDM2 and SIRT1 levels were upregulated in CD90-overexpressing AGS cells, compared with AGS cells transfected with the empty vector. In contrast, PTEN, p53, SIRT2, SIRT3 and SIRT6 were downregulated. The results indicate that CD90 affects the biological behavior and levels of energy metabolism of gastric cancer cells by targeting the PI3K/AKT/HIF-1α signaling pathway.[This corrects the article DOI 10.3892/ol.2015.3122.].The present study aimed to detect the immunoexpression and clinical significance of Porphyromonas gingivalis (P. gingivalis) in the tumor microenvironment (TME) of oral squamous cell carcinoma (OSCC). The immunoexpression of P. gingivalis in OSCC tissues was detected via immunohistochemistry (IHC) after P. gingivalis was infected into the TME of OSCC. To identify the differentially expressed genes in the carcinogenesis and progression of OSCC with P. gingivalis infection, microarray datasets (GSE87539 and GSE138206) were downloaded from the Gene Expression Omnibus database. The immunoexpression levels of C-X-C motif chemokine ligand 2 (CXCL2) and tumor-associated neutrophils (TANs) were also evaluated via IHC, and the immunoexpression levels of all three clinical variables were analyzed using χ2 or Fisher's exact tests. The survival rates were calculated using the Kaplan-Meier method and the survival curves were compared using log-rank tests. Predominantly strong immunoexpression of P. gingivalis was identified in OSCC samples.