This study investigates the expression of hypoxia-inducible factor-l alpha (HIF-1α) and carbonic anhydrase IX (CAIX) in nasopharyngeal carcinoma (NPC) tissues and their correlation with clinicopathological features and prognosis in NPC patients. The expression of HIF-1α and CAIX proteins was detected by immunohistochemical staining in 129 samples of NPC and 20 samples of chronic nasopharyngitis. The correlations between the expression of these two proteins and clinicopathological features and prognosis were evaluated in NPC patients. Our results showed that the positive expression rates of HIF-1α and CAIX proteins in NPC were significantly higher than those in chronic nasopharyngitis (both P < 0.01). In addition, high HIF-1α protein expression was correlated with lymph node metastasis and advanced clinical stage for NPC patients (both P < 0.01), whereas there were no findings of correlations between CAIX protein expression and gender, age, T stage, node involvement and clinical stage (all P > 0.05). The Spearman analysis indicated that HIF-1α was positively correlated with CAIX expression (r = 0.249, P = 0.004). HIF-1α and CAIX co-expression was associated with the poor overall survival (OS), progression-free survival (PFS), loco-regional relapse-free survival (LRRFS) and distant metastasis-free survival (DMFS) in NPC patients (P = 0.017, P = 0.022, P = 0.033, and P = 0.017, respectively). Multivariate analysis showed that the positive expression of CAIX protein was an independent prognostic factor for PFS, LRRFS and DMFS. In conclusion, overexpression of HIF-1α and CAIX might be involved in the carcinogenesis and development of NPC and they were associated with patients’ poor prognosis.

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The present study aimed to retrospectively analyze the survival outcomes and prognostic factors for patients with nasopharyngeal carcinoma (NPC) receiving intensity-modulated radiotherapy (IMRT). Clinical data was collected from 691 patients with NPC receiving IMRT from January 2009 to August 2015. A survival analysis was performed and prognostic factors were analyzed using the Kaplan–Meier method, the Cox proportional hazards regression model, and the log-rank test. The median follow-up time was 62.8 months. Sixty-three patients experienced relapse, 44 cases (70%) of which occurred within 3 years. Six cases (9.5%) remained in remission for over 5 years. Seventy-two patients developed metastasis, 63 cases (87.5%) of which occurred within 3 years and only 1 case occurred after 5 years (1.3%). Five-year disease special survival (DSS), progression free survival, locoregional recurrence free survival, and distant metastasis free survival were 86.5%, 82.5%, 90.7%, and 89.4%, respectively in patients with NPC. Patients with stage III NPC with and without induction chemotherapy had 5-year DSS rates of 95.8% and 89.3%, respectively ( P = .00). Patients with stage IVa NPC with and without induction chemotherapy had 5-year DSS rates of 73.1% and 68.9%, respectively ( P = .04). The 5-year DSS rates of patients with stage III with or without concurrent chemotherapy were 92.8% and 85.5%, respectively ( P = .04). The 5-year DSS rates of patients with stage IV with or without concurrent chemotherapy were 72.7% and 53.0% ( P = .02). IMRT improves the survival rate of patients with NPC. Recurrence and metastasis mainly occur within 2 to 3 years after radiotherapy. Induction and concurrent chemotherapy improve the 5-year DSS of patients with locally advanced NPC.

Long non-coding RNAs (lncRNAs) are involved in development of non-small cell lung cancer (NSCLC) by interacting with microRNAs (miRNAs) and/or mRNAs. However, the function of most lncRNAs in NSCLC remains unclear. Reverse transcription-quantitative PCR (RT-qPCR) and western blot were applied for detection of mRNA/miRNA and protein level. Interaction between LncRNA small nucleolar RNA host gene 14 (SNHG14) and miR-382-5p was validated by dual luciferase reporter assay. Cell proliferation and apoptosis was detected using Cell Counting Kit 8 (CCK8) and Flow cytometry, while cell migration and invasion was detected by scratch assay and Transwell assay. SNHG14 was upregulated in NSCLC tissues and cell lines. SNHG14 silencing reduced proliferation, migration and invasion, and induced apoptosis in A549 cells. SNHG14 was negatively correlated with miR-382-5p in NSCLC tissues, SNHG14 and miR-382-5p negatively regulated each other in A549 cells. SNHG14 promoted expression of miR-382-5p target genes, including LIM-only protein 3 (LMO3) and SET domain containing lysine methyltransferase 8 (SETD8), in A549 cells. miR-382-5p inhibition reversed SNHG14 knockdown-induced increase in apoptosis and decrease in proliferation, migration and invasion. SNHG14 was correlated with SETD8 and LMO3 in NSCLC tissues. Collectively, SNHG14 promoted NSCLC proliferation, migration and invasion, while inhibited apoptosis by sponging miR-382-5p in A549 cells.

Laryngeal squamous cell carcinoma (LSCC) is a highly invasive malignant tumor in the head and neck area. As an oncogene, long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes cell proliferation, migration and invasion several types of cancer. The present study aimed to reveal the effects of NEAT1 on the progression of LSCC. Reverse transcription-quantitative PCR (RT-qPCR) was used to detect relative mRNA expression levels of NEAT1, microRNA (miR)-204-5p and semaphorin (SEMA) 4B. Kaplan-Meier analysis was used to analyze overall survival times. RNA in-situ hybridization (ISH) exhibited the distribution of NEAT1 and miR-204-5p in tissues. RNA fluorescence ISH was used to analyze the distribution of NEAT1 and miR-204-5p in the cells. Western blot analysis was used to detect the expression level of target proteins. Cell viability was analyzed using a MTT assay, while flow cytometry was used to determine cell apoptosis. Wound healing and Transwell invasion assays were used to value cell migration and invasion, respectively. RNA immunoprecipitation assay, bioinformatics prediction and a dual luciferase reporter assay were used to analyze the target relationship. The RT-qPCR results showed that NEAT1 was highly expressed and miR-204-5p had decreased expression in LSCC tissues and cells compared with that in the normal tissue and the 16HBE-14o cell line, respectively. Knockdown of NEAT1 using small interfering (si) RNA and overexpressed miR-204-5p both effectively inhibited the proliferation, migration and invasion of LSCC cells. Besides, further experiments revealed that miR-204-5p was a target of NEAT1. At the same time, silenced miR-204-5p reversed the anti-tumor effects of si-NEAT1. In addition, SEMA4B was targeted by miR-204-5p in LSCC cells and upregulated SEMA4B weakened the antitumor effects of miR-204-5p in LSCC cells. NEAT1 regulated the expression of SEMA4B by targeting miR-204-5p in LSCC cells. Overall, NEAT1 promoted the proliferation and invasion of LSCC cells by regulating the miR-204-5p/SEMA4B axis.

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The radiation sensitivity of tumor cells is closely related to tumor cell hypoxia. Hypoxia-inducible factor-1α (HIF-1α) is considered a key transcription factor which regulates the sensitivity of hypoxic tumor cells to radiotherapy. On the other hand, some studies have shown that gold nanomaterials improve radiation sensitivity. However, studies on the effect of gold nanomaterials carrying HIF-1αsiRNA on tumor radiotherapy, and the underlying mechanisms are limited. Thus, the present study was aimed at investigating the effect of gold nanocomposites (AuNRs) carrying HIF-1αsiRNA (AuNRs-HIF-1αsiRNA) on the radiation sensitivity of nasopharyngeal carcinoma (NPC) hypoxia cells. The effect of AuNRs-HIF-1αsiRNA on radiation sensitivity of hypoxic NPC cells was determined under Xray irradiation. The results showed that Au-HIF-1αsiRNA improved the radio-sensitivity of NPC tumor. Thus, this study has demonstrated that gold nanomaterials carrying HIF-1αsiRNA effectively increased the radio-sensitivity of hypoxic tumor, thereby improving the effect of radiotherapy on NPC cells.