Journal of experimental & clinical cancer research : CR · 2017
CDC42-interacting protein 4 promotes metastasis of nasopharyngeal carcinoma by mediating invadopodia formation and activating EGFR signaling.
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Meng Dong-Fang, Xie Ping, Peng Li-Xia, Sun Rui, Luo Dong-Hua, Chen Qiu-Yan, Lv Xing, Wang Lin, Chen Ming-Yuan, Mai Hai-Qiang, Guo Ling, Guo Xiang, Zheng Li-Sheng, Cao Li, Yang Jun-Ping, Wang Meng-Yao, Mei Yan, Qiang Yuan-Yuan, Zhang Zi-Meng, Yun Jing-Ping, Huang Bi-Jun, Qian Chao-Nan
Аннотация
BACKGROUND: Nasopharyngeal carcinoma (NPC) is a common malignancy in Southern China and Southeast Asia. In this study, we investigated the functional and molecular mechanisms by which CDC42-interacting protein 4 (CIP4) influences NPC.
METHODS: The expression levels of CIP4 were examined by Western blot, qRT-PCR or IHC. MTT assay was used to detect the proliferative rate of NPC cells. The invasive abilities were examined by matrigel and transwell assay. The metastatic abilities of NPC cells were revealed in BALB/c nude mice.
RESULTS: We report that CIP4 is required for NPC cell motility and invasion. CIP4 promotes the activation of N-WASP that controls invadopodia formation and activates EGFR signaling, which induces downstream MMP2 (matrix metalloproteinase 2) upregulation. In addition, CIP4 could promote NPC metastasis by activating the EGFR pathway. In nude mouse models, distant metastasis was significantly inhibited in CIP4-silenced groups. High CIP4 expression is an independent adverse prognostic factor of overall survival (OS) and distant metastasis-free survival (DMFS).
CONCLUSION: We identify the critical role of CIP4 in metastasis of NPC which suggest that CIP4 may be a potential therapeutic target of NPC patients.
METHODS: The expression levels of CIP4 were examined by Western blot, qRT-PCR or IHC. MTT assay was used to detect the proliferative rate of NPC cells. The invasive abilities were examined by matrigel and transwell assay. The metastatic abilities of NPC cells were revealed in BALB/c nude mice.
RESULTS: We report that CIP4 is required for NPC cell motility and invasion. CIP4 promotes the activation of N-WASP that controls invadopodia formation and activates EGFR signaling, which induces downstream MMP2 (matrix metalloproteinase 2) upregulation. In addition, CIP4 could promote NPC metastasis by activating the EGFR pathway. In nude mouse models, distant metastasis was significantly inhibited in CIP4-silenced groups. High CIP4 expression is an independent adverse prognostic factor of overall survival (OS) and distant metastasis-free survival (DMFS).
CONCLUSION: We identify the critical role of CIP4 in metastasis of NPC which suggest that CIP4 may be a potential therapeutic target of NPC patients.
Предметные рубрики MeSH
AnimalsCarcinomaCell Line, TumorCell MovementCell ProliferationErbB ReceptorsFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeMicrotubule-Associated ProteinsMinor Histocompatibility AntigensNasopharyngeal CarcinomaNasopharyngeal NeoplasmsNeoplasm InvasivenessNeoplasm TransplantationPodosomesPrognosisSignal TransductionSurvival AnalysisWiskott-Aldrich Syndrome Protein, Neuronal