J Neurol Surg B Skull Base 2019; 80(S 01): S1-S244
DOI: 10.1055/s-0039-1679577
Oral Presentations
Georg Thieme Verlag KG Stuttgart · New York

The Role of MUC16 in Nasopharyngeal Carcinoma

Hai Zhao
1   The Affiliated Hospital of Qingdao University, Qingdao Shi, Shandong Sheng, China
,
Jianbao Ju
1   The Affiliated Hospital of Qingdao University, Qingdao Shi, Shandong Sheng, China
› Author Affiliations
Further Information

Publication History

Publication Date:
06 February 2019 (online)

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    Background: MUC16, a large molecular weight cell surface glycoprotein, is overexpressed in several types of cancer; however, its role in nasopharyngeal carcinoma and the association between MUC16 and Epstein–Barr virus remain unknown. In the present study, the role of MUC16 in nasopharyngeal carcinoma and the association between MUC16 and EBV were investigated.

    Methods: qRT-PCR and western blot analysis were conducted in cell lines and tumor samples. The clinical significance of MUC16 was evaluated using immunohistochemistry.

    Results: MUC16 was downregulated in the nasopharyngeal carcinoma tissues (Q34 and Q36) compared with the normal nasopharyngeal tissues (Q3, Q5, and Q6) which suggests that MUC16 is associated with the development of nasopharyngeal carcinoma at both the mRNA and protein levels (p < 0.05). In addition, the experimental data indicated that MUC16 was significantly down regulated in the EBV-positive NPC cell lines (C666) compared with the EBV-negative NPC cell lines (HONE, CNE), in the EBV-positive gastric carcinoma cell lines (GT38, GT39 and SUN719) compared with the EBV-negative gastric carcinoma cell lines (AGS, BGC-823 and SGC-7901) (p < 0.05). The immunohistochemistry staining indicated that MUC16 was located in the apical membrane of the ciliated cells of the normal nasopharyngeal epithelium. When comparing the MUC16 composite scores of the normal nasopharyngeal epithelium specimens with those of the NPC specimens, the difference was significant (p < 0.05). Based on these date, low expression of MUC16 may be associated with EBV infection.

    Conclusion: The findings of the present study indicate downregulated expression of MUC16 may be associated with NPC, and EBV infection may induce MUC16 downregulation at the mRNA and protein levels. Thus, MUC16 may participate in the development and progression of NPC, and may promote NPC through EBV infection. However, the specific mechanism and pathway between MUC16 and NPC, and MUC16 and EBV remain unknown. MUC16 may be used as a tumor marker for NPC in the future.


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    No conflict of interest has been declared by the author(s).