Histone Methyltransferase SUV39H2 Supports Nasopharyngeal Carcinoma Cell Metastasis by Regulation of SIRT1.

Nasopharyngeal carcinoma (NPC) is a malignant tumor with high metastatic features originating from the nasopharynx. However, the underlying mechanism of Suppressor of variegation 3-9 homolog 2 (SUV39H2) in NPC remains poorly understood. RT-qPCR was carried out to examine SUV39H2 and SIRT1 expression in NPC tissues and cells. Kaplan-Meier method was utilized to evaluate the association between SUV39H2 level and overall survival. The function of SUV39H2 and SIRT1 in NPC cell viability, metastasis, and apoptosis was tested through CCK-8, transwell, and flow cytometry experiments. Here, it was uncovered that SUV39H2 level was augmented in NPC tissues and cells. Moreover, SUV39H2 expedited NPC cell viability, metastasis, and inhibited apoptosis, while SIRT1 addition reversed these impacts. Besides, SUV39H2 induced H3K9me3 enhancement to repress SIRT1 transcription via binding to SIRT1 promoter. Collectively, our results demonstrated upregulated SUV39H2 aggravated NPC tumorigenesis through SIRT1, which may offer a potential therapeutic target for NPC.

MicroRNA-223-5p suppresses the progression of nasopharyngeal carcinoma by targeting DCLK1.

The aim of the present study was to investigate the function of microRNA (miR)-223-5p in the malignant biological behavior of nasopharyngeal carcinoma (NPC) and elucidate the underlying molecular mechanism. The expression levels of miR-223-5p and doublecortin-like kinase 1 (DCLK1) were detected via reverse transcription-quantitative PCR analysis. Cell viability was evaluated using Cell Counting Kit-8 assay. Cell migration and invasion were measured via Transwell assays, while a luciferase reporter assay was conducted to identify the interaction between miR-223-5p and DCLK1. The results demonstrated that miR-223-5p expression was significantly downregulated, whereas DCLK1 expression was significantly upregulated in NPC tissues and cells. Moreover, both miR-223-5p overexpression and DCLK1 silencing markedly suppressed the progression of NPC. It was also observed that miR-223-5p directly targeted DCLK1 and decreased its expression. Furthermore, it was suggested that DCLK1 overexpression may partially reverse the suppressive effects of miR-223-5p on the progression of NPC. Collectively, the results of the present study indicated that miR-223-5p may suppress NPC progression by targeting DCLK1, thereby indicating a novel potential approach to the diagnosis and treatment of NPC.

[Correlation of serum PTTG1 expression level with clinicopathological features and prognosis in patients with laryngeal cancer].

Objective:To investigate the correlation between the expression level of serum pituitary tumor transforming gene（PTTG1） and clinicopathological characteristics and prognosis in patients with laryngeal cancer. Method:Enzyme-linked immunosorbent assay was used to detect the expression of serum PTTG1 in 80 patients with laryngeal cancer and 60 patients with vocal cord polyps. The relationship between the clinicopathological characteristics of patients with laryngeal cancer and the expression of serum PTTG1 was analyzed. Cox regression analysis was used to analyze related factors affecting the prognosis of laryngeal cancer. Result:Serum PTTG1 expression level in patients with laryngeal cancer was significantly higher than that in patients with vocal cord polyps, and the difference was statistically significant（P<0.05）. The higher the lymph node metastasis, the higher the tumor TNM stage, and the lower the degree of differentiation, the higher the serum PTTG1 expression level（P<0.05）. In the prognostic survival analysis, univariate analysis showed that lymph node metastasis, tumor TNM stage, degree of differentiation, tumor diameter, and expression of PTTG1 were related to the prognosis of laryngeal cancer（P<0.01）. Cox regression multivariate showed lymph node metastasis（HR=2.651, 95%CI1.452-4.823, P=0.002）, high tumor TNM stage（HR=2.944, 95%CI1.155-6.189, P=0.026）, and low differentiation（HR=1.620, 95%CI1.133-2.169, P=0.003） and high PTTG1 expression（HR=3.511, 95%CI1.432-7.156, P<0.001） were risk factors affecting the prognosis of patients with laryngeal cancer. Conclusion:The expression level of serum PTTG1 may be closely related to the clinicopathological characteristics and prognosis of patients with laryngeal cancer, and its high expression may be one of the indicators of poor prognosis of patients with laryngeal cancer.

CircCTDP1 promotes nasopharyngeal carcinoma progression via a microRNA­320b/HOXA10/TGFß2 pathway.

Circular RNAs have been reported to play a vital role in the development and progression of various types of cancer. However, the underlying molecular role of circular RNA CTDP1 (circCTDP1) in the tumorigenesis of nasopharyngeal carcinoma (NPC) remains unknown. In the present study, circCTDP1 expression was found to be markedly upregulated in NPC tissues and cell lines (SUNE1, SUNE2 and 6­10B cell lines). Knockdown of circCTDP1 resulted in inhibition of proliferation, migration and invasion, and promoted apoptosis of NPC cells. Moreover, circCTDP1 directly interacted with microRNA (miR)­320b based on bioinformatics prediction and dual luciferase assay, and transfection with an miR­320b inhibitor reversed the effects of circCTDP1 knockdown on NPC cells. Furthermore, circCTDP1/miR­320b promoted NPC progression by regulating the expression of homeobox A10 (HOXA10). In addition, it was demonstrated that HOXA10 may exert its oncogenic role in NPC by regulating the expression of transforming growth factor ß2 (TGFß2). Taken together, these results revealed a novel regulatory mechanism, which may provide an improved understanding of NPC tumorigenesis and be useful in the development of potential targets for NPC therapy.

Elevated SUV39H2 attributes to the progression of nasopharyngeal carcinoma via regulation of NRIP1.

Nasopharyngeal carcinoma (NPC) is a prevalent tumor in southern China and southeast Asia. Recent studies have demonstrated that viral infection, somatic genetic changes, and epigenetic changes synergistically contribute to NPC pathogenesis. Genome-wide studies show that epigenetic aberrations likely drive nasopharyngeal carcinoma development and progression. This work is aimed at investigating the effect of histone methyltransferase SUV39H2 in NPC. The elevated expression of SUV39H2 in NPC is observed by analyzing GSE53819 and GSE12452 downloaded from the Gene Expression Omnibus (GEO) database. SUV39H2 knockdown inhibits NPC proliferation and induces the apoptosis of cancer cells. At last, RNaseq analysis identifies a variety of SUV39H2 downstream genes related with cancer, in which, NRIP1 is identified as a critical downstream target of SUV39H2 in NPC. Taken together, these findings provide a theoretical basis for understating the biological roles of SUV39H2 in NPC.