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The potential immunotherapy effect of Ginkgolide B thwarts oral squamous cell carcinoma progression by targeting the
De-Wei Lai1, Pei-Yi Chu2, Meei-Ling Sheu3
1Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan; Experimental Animal Center, Department of Molecular Biology and Cell Research, Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan.
Background:
Oral cancer is a malignant tumor of the oral cavity, with regulatory T cell (Treg) infiltration associated with poor prognosis. Ginkgolide B (GB) has demonstrated effects on lipid metabolism; however, its potential immunotherapeutic effects on oral cancer have not been elaborated.
Purpose:
This study aimed to explore the immunotherapeutic effects of Ginkgolide B (GB) in oral cancer.
Study Design:
We investigated the interactive mechanisms between Tregs and oral cancer cells in regulating sterol regulatory element-binding protein 1 (SREBP1)/ kallikrein-related peptidase 8 (KLK8)/ CC motif chemokine ligand 22 (CCL22) axis by GB treatment.
Methods:
Tissue array staining and the gene expression omnibus (GEO) database were used to identify the correlation between SREBP1/ KLK8/ CCL22 in oral cancer prognosis. The molecular effects of GB on SAS, KYSE-510, and TE-1 cells were examined by RNA sequencing. Electrophoretic mobility shift assay was used to analyse SREBF1/KLK8 transcription promoter activity. SREBP1 and KLK8 genetic engineering or recombinant proteins were used to evaluate CCL22 expression and Treg chemotactic response. An MOC-2-implanted mouse model was used to evaluate the therapeutic effects of GB and genetic engineering conditions.
Results:
Web-based visualization platform and tissue array data showed that SREBP1 expression was negatively correlated with oral cancer prognosis and SREBP1 and KLK8 positively correlated (R = 0.4648, p < 0.001). In addition, in vivo, ex vivo and in vitro experiments demonstrated that GB treatment or SREBP1 knockdown inhibited cancer cells proliferation, migration and Tregs chemotaxis. Mechanistically, GB treatment or SREBP1 knockdown attenuated SREBP1-regulated transcription of KLK8, reducing CCL22 secretion. Conversely, treatment with U18666a or SREBP1 transfection reversed these effects.
Conclusions:
GB is a novel SREBP1 inhibitor that effectively prevents immune escape by oral cancer cells through modulation of the SREBP1/KLK8/CCL22 axis, presenting a promising new approach for oral cancer immunotherapy.
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