The kinesin family member 18A protein was dysregulated in several human cancers and involved in cancer progression.However,the significance in oral tongue squamous cell carcinoma(OTSCC)has not been studied.The present...The kinesin family member 18A protein was dysregulated in several human cancers and involved in cancer progression.However,the significance in oral tongue squamous cell carcinoma(OTSCC)has not been studied.The present study was intended to explore the functions of KIF18A in oral tongue squamous cell carcinoma.The immunohistochemistry(IHC)assay was performed to assess the relationships between the KIF18A protein expression level and clinical-pathological features of the patients.The biological functions of KIF18A in OTSCC cells were investigated by the experiments in vitro and in vivo.Based on immunohistochemistry,we found that KIF18A was correlated with the clinical-pathological features of OTSCC patients.High expression of KIF18A was associated with the lymph node metastasis,and clinical stages.In vitro experiments revealed that silencing of KIF18A significantly inhibited the expression of the proliferation and migration related proteins such as Ki67,proliferating cell nuclear antigen,matrix metalloproteinase-7 and matrix metalloproteinase-9,and thereby inhibiting the proliferation,migration and invasion of tumor cells.In vivo,knocking-down of KIF18A could inhibit the tumor growth in nude mice.In conclusion,we found KIF18A promoted tumor progression in vivo and in vitro and might become an effective target for the treatment of OTSCC.展开更多
Objective:Osteosarcoma is a common primary highly malignant bone tumor.Kinesin family member 18B(K1F18B)has been identified as a potential oncogene involved in the development and metastasis of several cancer types.Wh...Objective:Osteosarcoma is a common primary highly malignant bone tumor.Kinesin family member 18B(K1F18B)has been identified as a potential oncogene involved in the development and metastasis of several cancer types.While KIF18B overexpression in osteosarcoma tissue is clearly detected,its specific function in the disease process remains to be established.Methods:K IF18B expression was assessed in osteosarcoma tissues and cells.We additionally evaluated the effects of KIF18B on proliferation,migration,and invasion of osteosarcoma cells,both in vitro and in vivo.Results:Our results showed overexpression of KIF18B in osteosarcoma tissues and cells.Knockdown of K IF18B induced G1/S phase arrest and significantly inhibited proliferation,migration,and invasion of osteosarcoma cells,both in vitro and in vivo.K IF18B regulated P-catenin expression at the transcriptional level by controlling nuclear aggregation of ATF2 and at the post-transcriptional level by interacting with the adenomatous polyposis coli(APC)tumor suppressor gene in osteosarcoma cells.Conclusions:KIF18B plays a carcinogenic role in osteosarcoma by regulating expression ofβ-catenin transcriptionally via decreasing nuclear aggregation of ATF2 or post-transcriptionally through interactions with APC.Our collective findings support the potential utility of KIF18B as a novel prognostic biomarker for osteosarcoma.展开更多
文摘The kinesin family member 18A protein was dysregulated in several human cancers and involved in cancer progression.However,the significance in oral tongue squamous cell carcinoma(OTSCC)has not been studied.The present study was intended to explore the functions of KIF18A in oral tongue squamous cell carcinoma.The immunohistochemistry(IHC)assay was performed to assess the relationships between the KIF18A protein expression level and clinical-pathological features of the patients.The biological functions of KIF18A in OTSCC cells were investigated by the experiments in vitro and in vivo.Based on immunohistochemistry,we found that KIF18A was correlated with the clinical-pathological features of OTSCC patients.High expression of KIF18A was associated with the lymph node metastasis,and clinical stages.In vitro experiments revealed that silencing of KIF18A significantly inhibited the expression of the proliferation and migration related proteins such as Ki67,proliferating cell nuclear antigen,matrix metalloproteinase-7 and matrix metalloproteinase-9,and thereby inhibiting the proliferation,migration and invasion of tumor cells.In vivo,knocking-down of KIF18A could inhibit the tumor growth in nude mice.In conclusion,we found KIF18A promoted tumor progression in vivo and in vitro and might become an effective target for the treatment of OTSCC.
基金grants from the National Natural Science Foundation of China(Grant No.81802689)China International Medical Foundation(Grant No.Z-2014-06-15331)Conflict of interest。
文摘Objective:Osteosarcoma is a common primary highly malignant bone tumor.Kinesin family member 18B(K1F18B)has been identified as a potential oncogene involved in the development and metastasis of several cancer types.While KIF18B overexpression in osteosarcoma tissue is clearly detected,its specific function in the disease process remains to be established.Methods:K IF18B expression was assessed in osteosarcoma tissues and cells.We additionally evaluated the effects of KIF18B on proliferation,migration,and invasion of osteosarcoma cells,both in vitro and in vivo.Results:Our results showed overexpression of KIF18B in osteosarcoma tissues and cells.Knockdown of K IF18B induced G1/S phase arrest and significantly inhibited proliferation,migration,and invasion of osteosarcoma cells,both in vitro and in vivo.K IF18B regulated P-catenin expression at the transcriptional level by controlling nuclear aggregation of ATF2 and at the post-transcriptional level by interacting with the adenomatous polyposis coli(APC)tumor suppressor gene in osteosarcoma cells.Conclusions:KIF18B plays a carcinogenic role in osteosarcoma by regulating expression ofβ-catenin transcriptionally via decreasing nuclear aggregation of ATF2 or post-transcriptionally through interactions with APC.Our collective findings support the potential utility of KIF18B as a novel prognostic biomarker for osteosarcoma.
