The aim of the present study was to examine the effect of fatty acid binding protein-5 (FABP-5) gene on the proliferation, apoptosis and invasion of human gastric cancer SGC-7901 cells. The viability, apoptosis and cell invasion of SGC-7901 cells before and after FABP5 knockdown were taken as the study objects, design and synthesis of siRNA interference sequence were conducted according to FABP-5 mRNA coding sequences, and SGC-7901 cells were transiently transfected. The human gastric cancer SGC-7901 cells were divided into three groups: FABP-5 siRNA group, negative control group and blank control group. FABP-5 gene mRNA and protein expression levels were detected by RT-PCR and western blot analysis. The CCK-8 assay was used to detect in vitro cell proliferation, flow cytometry (FCM) was used to detect changes in cell cycle and apoptosis in each group, TUNEL staining was used to detect apoptosis in each group, and the cell invasion chamber assay was used to detect cell invasiveness in each group. Each test was repeated three times. The results of the RT-PCR and western blot analysis showed that, expression of FABP-5 mRNA and protein in the FABP-5 siRNA group was significantly decreased compared with the negative and blank control groups. The cell growth rate in the FABP-5 siRNA group was significantly retarded, cell cycle was arrested in G0/G1 phase, the number of cells in S phase was reduced, and compared with the negative and blank control groups, the apoptotic rate in the FABP-5 siRNA group was significantly increased (P<0.01), while proliferation and invasiveness were significantly decreased (P<0.05). In conclusion, specific FABP-5 gene silencing may reduce the invasiveness of gastric cancer cells, inhibit cell proliferation, and arrest cell cycle in G0/G1 phase, resulting in a significant increase in apoptosis.

Cluster of differentiation (CD)133 is an important cell surface marker of glioma stem cells (GSCs). The transcription of the CD133 gene is controlled by five alternative promoters (P1, P2, P3, P4 and P5), which are expressed in a tissue-specific manner. In the present study, gene recombination technology was used to construct two types of gene expression vectors that contained the P1 promoter of the CD133 gene, which regulated either the neomycin-resistance gene or the herpes simplex virus thymidine kinase (HSV-TK) gene. Following the stable transfection of U251 glioblastoma cells with these two gene vectors, the cells expressing the P1 promoter that regulated the neomycin-resistance gene were named CD133 (+) cells, while the cells expressing the P1 promoter regulating the HSV-TK gene were called CD133 (-) cells. The expression of CD133 was detected by flow cytometry and reverse transcription-quantitative polymerase chain reaction. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to assess cell proliferation ability, while the cell cycle was analyzed by flow cytometry, and a clone formation test was performed to evaluate the invasive capability of the cells. The results demonstrated that, due to CD133 expression, the cell proliferation ability and the invasive capability of CD133 (+) cells were significantly higher than those of CD133 (-) cells. In conclusion, the present study successfully established a novel method of screening GSCs in U251 cells based on the P1 promoter of the CD133 gene.

The current study investigated the molecular mechanisms underlying pediatric acute lymphoblastic leukemia (ALL) and screened for small molecular drugs as supplementary drugs to aid current therapy. Gene expression data of Gene Expression Omnibus (GEO) DataSet GSE42221, which consists of 7 primary human B-precursor samples and 4 control B-cell progenitor lymphoblast samples from patients with pediatric ALL, were downloaded from the public GEO database. Linear Models for Microarray Analysis package for R statistical software was used to identify differentially expressed genes (DEGs). Subsequently, biclustering analysis of DEGs was performed using pheatmap package for R. Functional enrichment analysis of DEGs was conducted using the Database for Annotation, Visualization and Integrated Discovery tool. Additionally, Search Tool for the Retrieval of Interacting Genes software was used to screen protein-protein interactions (PPIs) of the DEGs, and Connectivity Map database was employed to obtain small-molecule drugs that were significantly associated with DEGs. In total, 116 genes were identified as DEGs in pediatric ALL, including 56 downregulated and 60 upregulated genes. Functional enrichment analysis identified that upregulated DEGs, including marker of proliferation Ki-67, cyclin F and nucleolar and spindle associated protein 1, were significantly enriched in mesenchymal cell differentiation and development processes, whilst downregulated DEGs, including bone marrow morphogenetic protein 2, semaphoring 3F and ephrin B1 were enriched in cell cycle process. Amongst the DEGs, 169 PPIs were identified. Notably, carbimazole and quinostatin were associated with DEGs. Additionally, a number of DEGs were targeted by the two drugs, including signal transducer and activator of transcription 3, nucleolar and spindle associated protein 1 and cell division cycle 20. Mesenchymal cell differentiation and development as well as cell cycle processes may be important for pediatric ALL. Quinostatin may be used as a potent supplementary drug for treating pediatric ALL.

Bladder cancer (BLCA) is a common malignancy of human urinary tract, whose prognosis is influenced by complex gene interactions. Immune response activity can act as a potential prognostic factor in BLCA. The present study established a prognostic model, based on the identification of tumor transcription factors (TFs) and immune-related genes (IRGs), and further explored their therapeutic potential in BLCA. The enrichment scores of 29 IRG sets, identified in The Cancer Genome Atlas BLCA tumor samples, were quantified by single-sample Gene Set Enrichment Analysis. The abundance of infiltrated immune cells in tumor tissues was determined using the Estimating Relative algorithm. Tumor-related TFs and IRGs signatures were retrieved using Least Absolute Shrinkage and Selection Operator Cox regression analysis. A prognostic gene network was built using Pearson's correlation analysis as a means of predicting the regulatory relationship between prognostic TFs and IRGs. A nomogram was devised to also predict the overall survival (OS) rate of patients with BLCA. Based on the Genomics of Drug Sensitivity in Cancer data, potential therapeutic drugs were identified upon analyzing the relationship between the expression level of prognostic genes and respective IC50 values. In vitro experiments were implemented for further validation. Respective TF binding profiles were acquired from the JASPAR 2020 database. The elevated infiltration of CD8+ T Cells was correlated with an improved OS of patients with BLCA. An innovative prognostic model for BLCA was then constructed that composed of nine putative gene markers: CXCL13, prepronociceptin, microtubule-associated protein tau, major histocompatibility class I polypeptide-related sequence B, prostaglandin E2 receptor EP3 subtype, IL20RA, proepiregulin, early growth response protein 1 and FOS-related antigen 1 (FOSL1). Furthermore, a theoretical basis for the correlation between the prognostic TFs and IRGs was reported. For this, 10 potentially effective drugs targeting the TFs in the present model for patients with BLCA were identified. It was then verified that downregulation of FOSL1 can lead to an enhanced sensitivity of the TW37 in T24 bladder cancer cells. Overall, the present prognostic model demonstrated a robust capability of predicting OS of patients with BLCA. Hence, the gene markers identified could be applied for targeted therapies against BLCA.

Cell-cycle-associated and expression-elevated protein in tumor (CREPT) functions as a cell cycle modulator that enhances the transcription of cyclin D1 by interacting with RNA polymerase II. CREPT has been identified to be overexpressed in various human cancer types; however, the expression and significance of CREPT in renal cell carcinoma (RCC) has remained largely elusive. In the present study, increased expression of CREPT was identified in 46.7% RCC tissues compared with adjacent normal tissue (31.1%; P=0.032) using immunohistochemistry. Furthermore, overexpression of CREPT was significantly associated with the Tumor-Node-Metastasis stage (χ2=11.967, P=0.001) and Fuhrman grade (χ2=15.453, P<0.001). In addition, increased expression of CREPT was associated with poor overall survival (P=0.021) and disease-free survival (P=0.015) of patients according to Kaplan-Meier analysis. Cellular function assays demonstrated that knockdown of CREPT in the 786-O and 769P RCC cell lines suppressed their proliferative, colony formation, migratory and invasive capacity and led to cell cycle arrest in the G1 phase. In addition, the western blotting analysis demonstrated that CREPT may control the cell cycle through downregulation of cyclin D1 and c-myc. Collectively, the overexpression of CREPT was indicated to be a negative prognostic factor for RCC, and CREPT may serve as a novel therapeutic target for the treatment of RCC.

An increased risk of renal cell carcinoma (RCC) has been linked with obesity and metabolic syndrome. However, the mechanisms by which lipid metabolic disorders affect the development of RCC remain unclear and highly controversial. Integrin-linked kinase (ILK) is a serine/threonine protein kinase involved in the regulation of tumor cell growth and angiogenesis. In the present study, the effect of free fatty acids in the promotion of RCC progression was investigated by upregulating ILK. Results of the MTT assay indicated that treatment of 786-O cells with oleic acid induced a concentration-dependent increase in cell viability. Flow cytometry analysis revealed that the effect of oleic acid on cell apoptosis was not significant. Following treatment with oleic acid, the expression of ILK, phospho-Akt and G protein-coupled receptor 40 (GPR40) was increased in 786-O cells. These effects were reversed when the expression of ILK was downregulated using specific small interfering RNA. These results indicate that free fatty acids are associated with the development of renal cell carcinoma via activation of the GPR40/ILK/Akt pathway, revealing a novel mechanism for the correlation between metabolic disturbance and renal carcinoma.

Oral squamous cell carcinoma is one of the most common causes of malignancy-associated death. Early diagnosis of oral squamous cell carcinoma (OSCC) is important in patient treatment and prognostic evaluation. Due to the lack of significant therapeutic benefit, the 5-year survival rate has not improved. Therefore, effective novel markers are needed to improve diagnosis. To determine novel promising diagnostic biomarkers for OSCC, 416 upregulated and 416 downregulated differentially expressed genes were screened from OSCC tissues using an RNA microarray. The results suggested that minichromosome maintenance protein (MCM5) mRNA was significantly overexpressed in OSCC tissues compared with that in adjacent normal tissues. Moreover, silencing of MCM5 expression an OSCC cell line (SCC-15) significantly impaired proliferation and colony formation. Furthermore, negative regulation of the mRNA and protein expression of MCM5 and demonstrated that MCM5 served as a cancer-promoting gene modulating OSCC cell proliferation through induced G2/M phase arrest. In this process, the mRNA expression of cyclin E and cyclin-dependent kinase 2 was downregulated, while p21 expression was upregulated. These results suggested that MCM5 may be an important pathogenic factor of OSCC. High expression levels of MCM5 may serve as a marker for the early diagnosis of OSCC.