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Treatment of recurrent head and neck squamous cell carcinoma (HNSCC) after radiotherapy (RT) with immune checkpoint inhibitors (ICIs) have attained certain success recently. However, some patients remained progressed and the total efficacy was finite, highlighting the need to identify new therapeutic options. DFNA5, also called GSDME, could switch chemotherapy drug induced-pyroptosis mediated by caspase-3. Presently, the relationship between DFNA5 and radiation in HNSCC remained unclear. Here, we showed that DFNA5 was up-regulated in HNSCC, and correlated with the expression of PD-L2, both of which reduced after the acquisition of radioresistance. Furthermore, PD-L1 was also tended to attenuate in radiation-resistant HNSCC. In sum, we showed that DFNA5 overexpressed in HNSCC and decreased with PD-L2 after attaining radiation-resistance, suggesting the potential role of DFNA5 as a possible combined target to amplify the immunotherapeutic efficacy in the future.
Keywords
DFNA5, head and neck squamous cell carcinoma, PD-L2, radioresistance, PD-L1
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A new preprint design is coming!
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 30 Mar, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Oncology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Treatment of recurrent head and neck squamous cell carcinoma (HNSCC) after radiotherapy (RT) with immune checkpoint inhibitors (ICIs) have attained certain success recently. However, some patients remained progressed and the total efficacy was finite, highlighting the need to identify new therapeutic options. DFNA5, also called GSDME, could switch chemotherapy drug induced-pyroptosis mediated by caspase-3. Presently, the relationship between DFNA5 and radiation in HNSCC remained unclear. Here, we showed that DFNA5 was up-regulated in HNSCC, and correlated with the expression of PD-L2, both of which reduced after the acquisition of radioresistance. Furthermore, PD-L1 was also tended to attenuate in radiation-resistant HNSCC. In sum, we showed that DFNA5 overexpressed in HNSCC and decreased with PD-L2 after attaining radiation-resistance, suggesting the potential role of DFNA5 as a possible combined target to amplify the immunotherapeutic efficacy in the future.
Figure 1
Figure 2
Figure 3
Figure 4
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