Background: Abnormal microangiogenesis and microenvironmental disturbances within the Nasopharyngeal carcinoma (NPC) can exacerbate tumor hypoxia, which may increase radiotherapy resistance and thus lead to poor prognosis in NPC patients. A non-invasive imaging technique, dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI), which can reflect the tumor blood perfusion and angiogenesis status, was used to investigate the relationships of DCE-MRI parameters with hypoxiainducible factor 1 alpha (HIF-1α) expression and tumor grades in NPC patients.Methods: 42 treatment-naive patients with pathologically confirmed NPC were enrolled in this analysis.Plain magnetic resonance scans and DCE-MRI scans were performed before treatment, and postprocessing was performed to calculate the relative enhancement (RE), maximum relative enhancement (MRE), maximum enhancement (ME), wash-in rate (WIR), wash-out rate (WOR), time to peak (TTP), and area under the curve (AUC). Immunohistochemistry was used to detect HIF-1α expression in electronasopharyngeal fiberoscopic specimens. The clinical grade/stage of NPC was jointly assessed by an experienced radiologist and a radiotherapist. The potential correlations of the DCE-MRI parameters with HIF-1α expression and clinical grades were analyzed. The statistical analysis was performed using SPSS 17.0 software package.Results: Among DCE-MRI parameters, RE, ME, and MRE were associated with the positive expression of HIF-lα in NPC and could reflect the hypoxic status in the local microenvironment of the cancer foci in vivo. RE, ME, and MRE were significantly higher in the positive HIF-1α expression group than in the negative HIF-1α expression group (F=5.

Hepatocellular carcinoma (HCC) is a common primary malignant tumor with a high mortality rate. Increasing evidence suggests that ribosomal protein LP1 (RPLP1) is involved in the progression of different types of cancer. Thus, the present study aimed to investigate the underlying molecular mechanism of RPLP1 in HCC progression. The cellular behaviors of Hep3b cells were assessed via Cell Counting Kit-8, colony formation, wound healing and Transwell assays. Western blot analysis was performed to detect protein expression levels, while reverse transcription-quantitative PCR analysis was performed to detect mRNA expression levels. The results demonstrated that RPLP1 was highly expressed in HCC tissues and cells, and the overexpression of RPLP1 was associated with a less favorable prognosis of patients with HCC. Notably, downregulation of RPLP1 significantly suppressed the proliferation, migration and invasion of Hep3b cells. Taken together, the results of the present study suggested that RPLP1 acts as an oncogene in HCC, and thus may be used to treat patients with HCC.

This study investigates the role of CPEB3 in esophageal cancer (EC) progression. The prognosis of EC patients was shown by survival analysis. CPEB3-targeting microRNAs were predicted by bioinformatics tools and further validated by dual-luciferase assay and RNA immunoprecipitation. CPEB3 expression in EC cell lines and EC tissues was analyzed by quantitative reverse transcription PCR. The viabilities of KYSE150 and EC9706 cells were measured by MTT and Cell Counting Kit-8 assays. The migration, invasion and tube formation of KYSE150 and EC9706 cells were examined by wound healing, Transwell and tube formation assay, respectively. E-cadherin, N-cadherin, fibronectin, vimentin and vascular endothelial growth factor (VEGF), epidermal growth factor receptor (EGFR) [and phosphorylation (p)] and STAT3 levels (and phosphorylation) in KYSE150 and EC9706 cells were determined by western blot analysis or quantitative reverse transcription PCR. In addition, a xenograft tumor model was established through subcutaneously implanting KYSE150 and EC9706 cells transfected with Lv-CPEB3 or Lv-control viruses. CPEB3 expression was downregulated in EC cells and tissues, and its overexpression inhibited viability, migration, invasion and the expressions of N-cadherin, fibronectin, vimentin and VEGF, EGFR, p-EGFR and p-STAT3 levels in KYSE150 cells, but promoted E-cadherin expression. Small interfering RNA (siRNA)-CPEB3 inversely affected these phenotypes and gene expressions in EC9706 cells. miR-106b-5p targeted CPEB3 and negatively regulated CPEB3 expression. miR-106b-5p mimics reversed the effect of CPEB3 overexpression on KYSE150 cells, and miR-106b-5p inhibitor reversed the effect of siRNA-CPEB3 on EC9706 cells. In mice, tumor volumes, weights and Ki-67 expression were lower in mice treated with Lv-CPEB3 than that with Lv-control. CPEB3 overexpressed by miR-106b-5p inhibition suppressed EC progression involved in EGFR and STAT3 signaling.