Search

Despite the recent development of treatment strategies for nasopharyngeal carcinoma, the effective management of this disease remains a challenging clinical problem. A better understanding of the regulatory roles of miR‐194 and mitogen‐activated protein kinase kinase kinase 3 (MAP3K3) in the nasopharyngeal‐carcinoma‐related gene network is required to address this issue. Here, we measured relative expression of miR‐194 in human nasopharyngeal carcinoma tissues and normal epithelial tissues by quantitative real time PCR. We transfected cultured CNE‐1 and C666‐1 cells with miR‐194 mimics, and then examined the effects on cell proliferation, cell migration and invasion. Luciferase reporter assay was used to validate the putative binding between miR‐194 and MAP3K3. We then examined the effect of knockdown and overexpression of MAP3K3 on cell tumorigenesis. Expression of miR‐194 is significantly down‐regulated in nasopharyngeal carcinoma specimens and tumor cell lines when compared with normal controls. In addition, miR‐194 suppressed tumor cell proliferation and viability, as well as migration and invasion of carcinoma cells. We found that miR‐194 binds the 3′ untranslated region of MAP3K3, and knockdown of miR‐194 inhibited nasopharyngeal carcinoma cell proliferation, migration and invasion. In accordance, overexpression of MAP3K3 reversed the inhibitory effects of miR‐194 in carcinoma cells. This study suggests that expression of miR‐194 is down‐regulated in nasopharyngeal carcinoma, and that miR‐194 can directly target MAP3K3 to regulate tumor progression. Given the pivotal involvement of MAP3K3 in nasopharyngeal carcinoma development, targeting miR‐194 may be a novel strategy for the treatment of nasopharyngeal carcinoma. miR‐194 was down‐regulated in nasopharyngeal carcinoma. miR‐194 can directly target MAP3K3 for regulating tumor progression. Given the pivotal involvement of MAP3K3 in nasopharyngeal carcinoma development, targeting miR‐194 could provide a novel strategy for the treatment of nasopharyngeal carcinoma. [ABSTRACT FROM AUTHOR]

Despite the recent development of treatment strategies for nasopharyngeal carcinoma, the effective management of this disease remains a challenging clinical problem. A better understanding of the regulatory roles of miR-194 and mitogen-activated protein kinase kinase kinase 3 (MAP3K3) in the nasopharyngeal-carcinoma-related gene network is required to address this issue. Here, we measured relative expression of miR-194 in human nasopharyngeal carcinoma tissues and normal epithelial tissues by quantitative real time PCR. We transfected cultured CNE-1 and C666-1 cells with miR-194 mimics, and then examined the effects on cell proliferation, cell migration and invasion. Luciferase reporter assay was used to validate the putative binding between miR-194 and MAP3K3. We then examined the effect of knockdown and overexpression of MAP3K3 on cell tumorigenesis. Expression of miR-194 is significantly down-regulated in nasopharyngeal carcinoma specimens and tumor cell lines when compared with normal controls. In addition, miR-194 suppressed tumor cell proliferation and viability, as well as migration and invasion of carcinoma cells. We found that miR-194 binds the 3' untranslated region of MAP3K3, and knockdown of miR-194 inhibited nasopharyngeal carcinoma cell proliferation, migration and invasion. In accordance, overexpression of MAP3K3 reversed the inhibitory effects of miR-194 in carcinoma cells. This study suggests that expression of miR-194 is down-regulated in nasopharyngeal carcinoma, and that miR-194 can directly target MAP3K3 to regulate tumor progression. Given the pivotal involvement of MAP3K3 in nasopharyngeal carcinoma development, targeting miR-194 may be a novel strategy for the treatment of nasopharyngeal carcinoma.

Purpose: To investigate the impact of chemotherapy and/or radiotherapy on disease-free survival (DFS) and overall survival (OS) rates of patients with thymic carcinoma after complete resection., Methods: Between 2001 and 2013, 54 patients with complete resection of thymic carcinoma in Hangzhou Cancer Hospital were retrospectively reviewed. The Kaplan-Meier method was used to evaluate the survival rates. The Cox proportional hazard model was used for multivariate analysis., Results: Among the 54 patients, Masaoka stage I was observed in seven patients, II in 22 patients, and III in 25 patients. Sixteen patients received adjuvant chemotherapy (six with chemotherapy alone and ten with radiotherapy and chemotherapy), 25 patients received adjuvant radiotherapy, and 13 patients did not receive radiotherapy and/or chemotherapy. The 5-year DFS and OS rates for all patients were 63.0% and 73.4%, respectively. Univariate analysis revealed that radiotherapy was significantly associated with DFS and OS (P=0.014 and P=0.029, respectively), while adjuvant chemotherapy was not (P=0.122 and P=0.373, respectively). Multivariate analysis showed that adjuvant radiotherapy increased DFS (P=0.041), but not OS (P=0.051)., Conclusion: Complete resection followed by adjuvant radiotherapy increased disease-free rates of thymic carcinoma patients.