Steroid receptor coactivator 1 (Src-1) and Twist1 are aberrantly upregulated in a variety of tumors and play an important role in tumor progression. However, the exact role of Src-1 and Twist1 in nasopharyngeal carcinoma (NPC) is uncertain. In this study, we investigated the possible prognostic value and biological effect of Src-1 and Twist1 in NPC. Src-1 and Twist1 expression was detected in a cohort of NPC patients (n = 134) by qRT-PCR. Kaplan-Meier survival analysis was used comparing overall survival (OS) and progression-free survival (PFS). Multivariate analysis was performed using the Cox proportional hazard regression model. Biologic effect of Src-1 and Twist1 in NPC cell lines was evaluated by western blot, colony formation assay, soft agar assay, scratch wound healing assay, transwell invasion assay and tumor xenografts growth. We have found that Src-1 and Twist1 were aberrantly upregulated in human NPC tissues, and associated with advanced tumor stage, distant metastasis and unfavorable prognosis. Knockdown of Src-1 or Twist1 in human NPC cell line CNE-1 suppressed colony formation, anchorage-independent growth, cell migration, invasion and tumor xenografts growth, while enforced expression of Src-1 or Twist1 in human NPC cell line HNE-2 promotes anchorage-independent growth, cell migration and invasion. In addition, Src-1 and Twist1 could suppress E-cadherin expression and increase Vimentin expression, thus suggested that Src-1 and Twist1 enhanced the malignant behaviors of NPC cells via inducing epithelial-mesenchymal transition (EMT). Our data indicated that Src-1 and Twist1 could be possible prognostic biomarkers and potential therapy targets for patients with NPC.
Laryngeal squamous cell carcinoma (LSCC) is the main pathological type of laryngeal cancer, which attacks the head and neck.
Chitosan dressing might be promising to promote the recovery following endoscopic sinus surgery (ESS). However, the results remain controversial. We conducted a systematic review and meta-analysis to explore the influence of chitosan dressing on ESS. PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases were systematically searched. Randomized controlled trials (RCTs) assessing the effect of chitosan dressing on endoscopic sinus surgery were included. Two investigators independently searched articles, extracted data, and assessed the quality of included studies. The primary outcomes were synechia and hemostasis. Meta-analysis was performed using random-effect model. Four RCTs involving 268 patients were included in the meta-analysis. Overall following ESS, compared with control intervention, chitosan dressing significantly reduced synechia (RR = 0.25; 95% CI 0.13-0.49; P < 0.0001) and promoted hemostasis (RR = 1.70; 95% CI 1.37-2.11; P < 0.00001), but showed no impact on granulations (RR = 1.18; 95% CI 0.72-1.95; P = 0.52), mucosal edema (RR = 0.88; 95% CI 0.60-1.29; P = 0.51), crusting (RR = 0.85; 95% CI 0.48-1.53; P = 0.60), and infection (RR = 0.88; 95% CI 0.51-1.52; P = 0.64). Compared to control intervention, chitosan dressing could significantly decrease edema and improve hemostasis, but had no effect on granulations, mucosal edema, crusting and infection.
Nasopharyngeal carcinoma (NPC) is a malignant tumor which is commonly found in East Asia and Africa. The present clinical treatment of NPC is still mainly based on chemotherapeutics and is prone to drug resistance and adverse reactions. Shikonin has been demonstrated to play the antitumor effect in various cancers. However, the specific effects and related regulatory mechanism of Shikonin in NPC have not been clearly declared yet. Cell viability was valued through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and cell proliferation was detected through colony formation assay and Bromodeoxyuridine (BrdU) assay. Hochest 33258 staining was used to value cell apoptosis. Cell migration and invasion were valued through wound healing and transwell invasion assay, respectively. Glucose uptake, lactate release, ATP level and pyruvate kinase M2 isoform (PKM2) activity were measured using corresponding assay kits. Western blotting was used to examine the expression of proteins related to cell proliferation, cell apoptosis, cell migration and the phosphatidylinositol 3 kinase (PI3K)/AKT signal pathway. We found that Shikonin treatment effectively suppressed cell proliferation and induced obvious cell apoptosis compared with the control. Besides, Shikonin treatment suppressed cell migration and invasion effectively. The detection about glycolysis showed that Shikonin treatment suppressed cell glucose uptake, lactate release and ATP level. The activity of PKM2 was also largely inhibited by Shikonin. Further study revealed that the PI3K/AKT signal pathway was inactivated by Shikonin treatment. In addition, the inducer of the PI3K/AKT signal pathway largely abolished the antitumor effect of Shikonin on cell proliferation, cell apoptosis, cell mobility and aerobic glycolysis in NPC cells. Shikonin inhibits growth and invasion of NPC cells through inactivating the PI3K/AKT signal pathway.
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