TRAF2 Knockdown in Nasopharyngeal Carcinoma Induced Cell Cycle Arrest and Enhanced the Sensitivity to Radiotherapy.

TRAF2 is a crucial adaptor protein involved in various signaling pathways. However, its biological functions in nasopharyngeal carcinoma (NPC) remain largely unknown. In the present study, we found that TRAF2 was overexpressed in nasopharyngeal carcinoma (NPC) cells. Knockdown of TRAF2 with shRNA si...

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Publicado en:BioMed Research International pp. 1 - 11
Autores principales: Zhu, Hongyuan, Ding, Weijun, Wu, Jiaojiao, Ma, Rongyou, Pan, Zhaohu, Mao, Xinli
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell 5/30/2020
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 5/30/2020
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        143503500
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        143503500
        10.1155/2020/1641340
        143503500
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        atl: TRAF2 Knockdown in Nasopharyngeal Carcinoma Induced Cell Cycle Arrest and Enhanced the Sensitivity to Radiotherapy.
      aug:
        au:
          Zhu, Hongyuan
          Ding, Weijun
          Wu, Jiaojiao
          Ma, Rongyou
          Pan, Zhaohu
          Mao, Xinli
        affil: Department of Otolaryngology, Affiliated Tai Zhou Hospital of Wenzhou Medical University, No. 150 Ximen Road, Linhai, Taizhou 317000, China
      sug:
        subj:
          Nasopharyngeal Carcinoma Radiotherapy
          Tumor Necrosis Factor Metabolism
          RNA Metabolism
          Cell Cycle Evaluation
          Gene Expression Evaluation
          Cell Proliferation Evaluation
          Human
          Xenografts
          Transcription Factors Metabolism
          Nasopharyngeal Carcinoma Prevention and Control
      ab: TRAF2 is a crucial adaptor protein involved in various signaling pathways. However, its biological functions in nasopharyngeal carcinoma (NPC) remain largely unknown. In the present study, we found that TRAF2 was overexpressed in nasopharyngeal carcinoma (NPC) cells. Knockdown of TRAF2 with shRNA significantly suppressed NPC cell proliferation and colony formation. The growth of xenograft tumor significantly reduced after TRAF2 was silenced. Conversely, the ectopic overexpression of TRAF2 significantly promoted cell proliferation and anchorage-independent growth. In TRAF2 knockdown cells, EGF-induced activation of transcriptional factors, including MSK1, CREB, and ATF2, markedly decreased. Accordingly, the transcriptional activity of AP-1 was substantially decreased in TRAF2-deficient cells. With the suppression of gene transcription, the expression of cyclin D1 was significantly impaired, which gave rise to the G0/G1 cell cycle arrest. Moreover, the overexpression of TRAF2 in NPC cells was associated with resistance to irradiation, and the potency of irradiation was substantially enhanced after TRAF2 was knocked down. Briefly, our studies demonstrated that TRAF2 had a crucial role in NPC development, and it might be of great potential to targeting TRAF2 for NPC prevention and treatment.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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