329P - High-level expression of HDAC10 is associated with PD-L1 expression and poor prognosis in patients with non-small cell lung cancer receiving pulmonectomy

Background

Recent studies showed that stimulation of HDACs could induce PD-1 dynamic expression on DCs, macrophages, colonic stromal cells, and cancer cells. Surprisingly, it is little is known about the specific expression of important HDAC10 in NSCLC tissue. In this study, we evaluated the expression level of HDAC10 and the correlation of HDAC10 and PD-L1 in NSCLC tissues and analyzed the predicting role of HDAC10 in cancer cells on postoperative survival in NSCLC patients receiving pulmonary lobectomy.

Methods

A total of 180 NSCLC patients receiving complete pulmonary resection and systematic lymph node dissection between April 2004 and August 2009 were enrolled. All the patients had integrated clinicopathological records and follow-up data. HDAC10 and PD-L1 expression on NSCLC samples were determined by using immunohistochemistry.

Results

Our results showed that HDAC10 expression level in cancer tissue was significantly higher than that in para-cancer tissue. HDAC10 expression level was also positively correlated with the PD-L1 expression level (r = 0.213, P < 0.05). Multivariate analysis showed that expression level of HDAC10 was an independent prognostic factor and HDAC10 overexpression indicated a poor overall survival in pulmonary carcinoma (r = 0.540, P < 0.001).

Conclusions

To our knowledge, this is the first time to associate HDAC10 with lung cancer patients’ survival status and to explore correlation between HDAC10 and PD-L1 expression. Our findings indicated that HDAC10 could be a valuable predicting marker that might provide help for clinicians to design effective therapeutic modality against NSCLC. Treatment response might be especially prominent in patients overexpressing HDAC10 in cancer cells. Our study suggest clinical relevance for the immune effects of HDAC10 and provide a rationale for the clinical evaluation of PD-L1 blockade in combination with HDAC10 inhibition.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

 The First Affiliated Hospital of Jinzhou Medical University.

Funding

This study was supported by the CSCO-HANSOH PHARMA Science Foundation of China (number Y-HS2019-29).

Disclosure

The author has declared no conflicts of interest.