Knockdown of FKBP3 suppresses nasopharyngeal carcinoma cell growth, invasion and migration, deactivated NF-κB/IL-6 signaling pathway through inhibiting histone deacetylase 2 expression.

Nasopharyngeal carcinoma (NPC) is a prevalent malignant tumor worldwide. FKBP3 has been reported to participate in tumorigenesis. Nevertheless, the role and mechanism of FKBP3 in NPC remains unclear. In this study, FKBP3 expression was observed to upregulate in NPC patients and cells. Moreover, knockdown of FKBP3 suppressed cell growth, invasion, and migration in HK1 and C666-1 cells. Mechanically, FKBP3 could enhance the p-p65 expression and activated p65 signaling pathway and increased interleukin-6 (IL-6) expression through enhancing histone deacetylase 2 (HDAC2) expression. In rescued experiment, the overexpression of HDAC2 restored diminished cell growth, invasion, and migration caused by FKBP3 depletion. In summary, the knockdown of FKBP3 suppressed NPC cell growth, invasion and migration, deactivated nuclear factor-κB/IL-6 signaling pathway through inhibiting HDAC2 expression, providing a potential therapeutic strategy for NPC treatment.

GTSE1 promotes nasopharyngeal carcinoma proliferation and angiogenesis by upregulating STMN1.

BACKGROUND: Nasopharyngeal carcinoma (NPC) is a malignant tumor with poor survival rate. G2 and S phase-expressed-1 (GTSE1) takes part in the progression of diverse tumors as an oncogene, but its role and potential mechanism in NPC remain unknown. METHODS: The GTSE1 expression was analyzed by western blot in NPC tissues and cells. Knock-down experiments were conducted to determine the function of GTSE1 in NPC by cell counting kit-8, the 5-ethynyl-2'-deoxyuridine (EdU) incorporation experiment, cell scratch wound-healing experiment, transwell assays, tube forming experiment and western blot. In addition, the in vivo role of GTSE1 was addressed in tumor-bearing mice. RESULTS: The expression of was increased in NPC. Silencing of GTSE1 suppressed cell viability, the percent of EdU positive cells, and the number of invasion cells and tubes, but enhanced the scratch ratio in NPC cells. Mechanically, downregulation of GTSE1 decreased the expressions of FOXM1 and STMN1, which were restored with the upregulation of FOXM1. Increased expression of STMN1 reversed the effects of the GTSE1 silencing on proliferation, migration, invasion and angiogenesis of NPC cells. Furthermore, knockdown of GTSE1 repressed the tumor volume and tumor weight of xenografted mice. CONCLUSION: GTSE1 was highly expressed in NPC, and silencing of GTSE1 ameliorated the malignant processes of NPC cells by upregulating STMN1, suggesting a possible therapeutical target for NPC.

[Clinical analysis of primary nasal sinus osteoma].

OBJECTIVE: To summarize and analyze the clinical features, diagnosis, surgical approaches and treatment outcomes of patients with primary nasal sinus osteoma. METHODS: A retrospective review of 48 cases with primary nasal sinus osteoma treated from January 2007 to December 2013 was performed. All patients underwent preoperative CT scan and postoperative histopathologic examination. The surgical approaches included lateral rhinotomy in 14 cases, nasal endoscopic resection in 12 cases, coronal surgical incision craniotomy in 13 cases, combined craniofacial approach in 4 cases, and Caldwell-Luc approach in 5 cases. RESULTS: The postoperative pathological diagnosis consisted of 3 variants, including 20 for compact type and 15 for cancellous type, and 13 for mixed type. Six cases were lost to follow-up and 42 cases were followed up for 6-60 months, 5 cases recurred. The post-operative complications included sinus mucous cyst in 4 cases, cerebrospinal fluid leak in 3 cases. CONCLUSIONS: Nasal sinus osteoma are common. CT or MRI is helpful to evaluate the osteoma size, location and possible sources, and to make operation scheme. Surgery is the first choice for sinus osteoma. Lateral rhinotomy and nasal endoscopic resection can be applied to most sinus osteoma. The prognosis of sinus osteoma is good, with fewer recurrence.