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The EC1.5 value (i.e., the concentration at which a test chemical induces a CD69 RFI of 1.5) may be used to assess skin sensitization potency of a chemical. This work may contribute to the development of an in vitro assay for skin sensitization based on the activation of T cells.Post‑transcriptional mechanisms are an important approach in the treatment of cancer, and may also be hijacked by tumor cells to help adapt to the local microenvironment. Filamin B (FLNB), an actin‑binding protein that provides crucial scaffolds for cell motility and signaling, has also been identified as an RNA‑binding protein. Recent studies demonstrated that FLNB might play an important role, not only in skeletal development, but also in regulating tumorigenesis; however, the effects of dysregulated expression of FLNB at the molecular level are not clear. In the present study, RNA‑sequencing was performed to analyze changes in overall transcriptional and alternative splicing between the knocked‑down FLNB and the control in HeLa cells. Decreased FLNB levels resulted in significantly lower apoptosis compared with control cells. FLNB knockdown extensively regulated the expression of genes in cell apoptosis, tumorigenesis, metastases, transmembrane transport and cartilage development. Moreover, FLNB regulated nsight for the current understanding of the mechanisms of FLNB‑mediated gene regulation.Long non‑coding RNAs (lncRNAs) have critical functions in non‑small cell lung cancer (NSCLC) growth. In the present study, we showed that lncRNA‑CCAT1 was upregulated in NSCLC tissues. High expression of lncRNA‑CCAT1 was related to tumor growth and reduced survival rate. We used short hairpin RNAs (shRNAs) to inhibit the expression of lncRNA‑CCAT1 in NSCLC cells. In vitro and in vivo results demonstrated that lncRNA‑CCAT1 knockdown suppressed tumor proliferation and induced apoptosis. Furthermore, microRNA‑218 (miR‑218) was confirmed as an effective target of lncRNA‑CCAT1 in NSCLC. CFI-402257 B lymphoma Mo‑MLV insertion region 1 homolog (BMI‑1), which served as a downstream target of miR‑218, was also inhibited by lncRNA‑CCAT1 knockdown. In conclusion, the present study indicated that upregulation of lncRNA‑CCAT1 in NSCLC is associated with tumor malignant potential. lncRNA‑CCAT1 enhances tumor growth in NSCLC by directly inhibiting miR‑218 and indirectly increasing BMI‑1 expression.Preeclampsia (PE) is a pregnancy-specific syndrome that has severe implications on perinatal mortality and morbidity. Excessive apoptosis of trophoblasts induced by hypoxia may be associated with the development of PE, but the exact pathogenesis is unknown. Forkhead box O transcription factor 3a (FOXO3a) is activated under hypoxic conditions. Furthermore, hypoxia‑inducible factor‑1α (HIF‑1α) is sensitive to variations in partial oxygen pressure. Thus, the aims of the present study were to investigate the expression levels of HIF‑1α and FOXO3a in placental samples of early onset severe PE, and their effect on trophoblastic apoptosis under hypoxic conditions. Cobalt chloride was used to establish the hypoxic model. The present study examined the expression levels of HIF‑1α and FOXO3a in the placental tissues and HTR8/SVneo cells under hypoxic conditions. It was found that HIF‑1α and FOXO3a were highly expressed in placental tissues of patients with PE and in HTR8/SVneo cells under hypoxic conditions. Furthermore, knockdown of FOXO3a using a specific small interfering RNA (siRNA) decreased apoptosis in HTR8/SVneo cells. Moreover, it was found that after knockdown of HIF‑1α using siRNA, FOXO3a expression and the apoptotic rate were reduced in HTR8/SVneo cells. Therefore, the present results indicated that the elevated expression of HIF‑1α increased trophoblastic apoptosis by regulating FOXO3a, which may be involved in the pathogenesis of PE.Radiotherapy and chemotherapy are two major treatment options for esophageal carcinoma, and heterogeneous treatment effects are observed in the clinical setting to provide an overall 5‑year survival rate of ~20%. Hence, defining the molecular mechanisms that affect the chemoradiotherapy response is vital to achieve an optimal outcome. The present study revealed that miR‑155‑5p may be involved in esophageal squamous cell carcinoma (ESCC). By means of reverse transcription‑PCR, the present study defined its differential expression pattern in six ESCC cell lines that were associated with resistance to radiation. Ectopic expression of miR‑155‑5p promoted DNA damage repair and induced resistance against radiation by non‑homologous end joining repair. It also enhanced chemoresistance, proliferation, and migration and invasion of ESCC cells. By further screening its potential target genes, the present study identified MAP3K10 as the direct target gene to exert its anti‑chemoradiation functions. The results also demonstrated that its differential expression pattern was negatively regulated by the methylation status of the upstream CpG island. Overall, the results of the present study demonstrated that miR‑155‑5p is a key molecule for understanding the heterogeneous responses of ESCC to chemoradiotherapy, and may be used in personalized treatment plans for this high mortality tumor in the future.Patients with hepatocellular carcinoma (HCC) have different prognoses depending on whether or not they also have fibrosis. Since long non‑coding RNAs (lncRNAs) affect tumor formation and progression, the present study aimed to investigate whether their expression might help predict the survival of patients with HCC. Expression profiles downloaded from The Cancer Genome Atlas database were examined to identify lncRNAs differentially expressed (DElncRNAs) between HCC patients with or without fibrosis. These DElncRNAs were then used to develop a risk scoring system to predict overall survival (OS) or recurrence‑free survival (RFS). A total of 142 significant DElncRNAs were identified using data from 135 patients with fibrosis and 72 without fibrosis. For HCC patients with fibrosis, a risk scoring system to predict OS was constructed based on five lncRNAs (AL359853.1, Z93930.3, HOXA‑AS3, AL772337.1 and AC012640.3), while the risk scoring system to predict RFS was based on 12 lncRNAs (PLCE1‑AS1, Z93930.3, LINC02273, TRBV11‑2, HHIP‑AS1, AC004687.