Reduced QSOX1 enhances radioresistance in nasopharyngeal carcinoma

Lei Zhou1, Hong-Min Chen1, Song Qu1,2,3

  • 1Department of Radiation Oncology, Affiliated Tumor Hospital of Guangxi Medical University and Cancer Institute of Guangxi Zhuang Autonomous Region, Nanning, Guangxi, P.R. China.

Oncotarget
|February 10, 2018
PubMed

Insights

Lower QSOX1 protein levels correlate with radioresistance in nasopharyngeal carcinoma (NPC). Suppressing QSOX1 in NPC cells reduces radiosensitivity, apoptosis, and metastasis, suggesting QSOX1 as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Radiotherapy Research

Background:

  • Nasopharyngeal carcinoma (NPC) treatment failure is often due to radioresistance.
  • Previous work identified QSOX1 as differentially expressed in NPC cells with varying radiosensitivities.

Purpose of the Study:

  • To investigate the biological role of QSOX1 in NPC.
  • To determine QSOX1's impact on NPC radiosensitivity and treatment outcomes.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC) to quantify QSOX1 levels in patient samples.
  • Small hairpin RNA (shRNA) to knockdown QSOX1 in CNE-2 NPC cells.
  • In vitro assays (colony formation, CCK-8, flow cytometry, transwell) and in vivo xenograft models to assess radiosensitivity, apoptosis, migration, and invasion.

Main Results:

  • Markedly lower QSOX1 levels were observed in radioresistant NPC patient sera and tissues compared to radiosensitive samples.
  • Knockdown of QSOX1 significantly increased cell survival under irradiation, reducing radiosensitivity.
  • QSOX1 silencing decreased apoptosis rates post-irradiation and suppressed cellular migration and invasion.
  • Xenograft models confirmed QSOX1 knockdown's role in promoting tumor growth and radioresistance.

Conclusions:

  • QSOX1 expression is inversely correlated with radiosensitivity in NPC.
  • Targeting QSOX1 presents a potential strategy to enhance NPC radiosensitivity and improve radiotherapy efficacy.

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