gms | German Medical Science

88. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e. V.

Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e. V.

24.05. - 27.05.2017, Erfurt

Silencing of FANCD2 enhances the radiosensitivity of metastatic cervical lymph node-derived head and neck squamous cell carcinoma HSC-4 cells

Meeting Abstract

  • corresponding author Gang Qin - Department of Otolaryngology Head and Neck Surgery, the Affiliated Hospital of S, Luzhou, China
  • Huajun Feng - Department of Otolaryngology Head and Neck Surgery, the Affiliated Hospital of S, Luzhou, China
  • Yilin Bao - Department of Otolaryngology Head and Neck Surgery, the Affiliated Hospital of S, Luzhou, China
  • Zhuoping Liang - Department of Otolaryngology Head and Neck Surgery, the Affiliated Hospital of S, Luzhou, China
  • Feipeng Zhao - Department of Otolaryngology Head and Neck Surgery, the Affiliated Hospital of S, Luzhou, China
  • Shengen Xu - Department of Otolaryngology Head and Neck Surgery, the Affiliated Hospital of S, Luzhou, China
  • Wei Xu - Department of Otolaryngology Head and Neck Surgery, the Affiliated Hospital of S, Luzhou, China
  • Chong Zhao - Department of Otolaryngology Head and Neck Surgery, the Affiliated Hospital of S, Luzhou, China

Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie. 88. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie. Erfurt, 24.-27.05.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. Doc17hno183

doi: 10.3205/17hno183, urn:nbn:de:0183-17hno1833

Veröffentlicht: 13. April 2017

© 2017 Qin et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Introduction: Fanconi anemia complementation group D2(FANCD2) is involved in the key steps of the Fanconi anemia (FA) pathway, which plays a role in the repair of DNA crosslink damage. However, the role of FANCD2 during radiotherapy for head and neck squamous cell carcinoma(HNSCC) is unclear.

Methods: Western blot was used to detect the expression of the FANCD2 in HSC-4 cells. Through in vitro and in vivo experiments, the impact of FANCD2 shRNA interference on the radiosensitivity of HSC-4 cells was investigated. TUNEL, Western blot and immunohistochemistry were used to analyze the expression of apoptotic proteins and proteins involved in apoptosis-related pathways after radiotherapy to investigate the relevant mechanism of increased radiosensitivity of HSC-4 cells induced by the silencing of FANCD2.

Results: In vitro, the silencing of FANCD2 inhibited cell proliferation, decreased the survival rate, increased apoptosis and induced S phase arrest in HSC-4 cells after radiotherapy. In vivo, the silencing of FANCD2 could prolong the tumor-forming time and slow the tumor growth. In addition, the tumor volume was reduced, the weight was deceased, and the tumor inhibition rate was increased after radiotherapy. TUNEL showed that the silencing of FANCD2 increased the apoptosis in HSC-4 cells induced by radiotherapy. Both in vitro and in vivo experiments revealed that the expression of Bax and p-p38 proteins in HSC-4 cells, in which FANCD2 had been silenced, was increased after radiotherapy, whereas the expression of p38 and Bcl2 proteins was decreased.

Conclusions: The silencing of FANCD2 enhanced the radiosensitivity of HSC-4 cells, and its mechanism is related to the activation of the p38 MAPK signaling pathway and to the regulation of the expression of Bax and Bcl2 proteins.

Unterstützt durch: The Affiliated Hospital of Southwest Medical University

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