Vincristine upregulates PD-L1 and increases the efficacy of PD-L1 blockade therapy in diffuse large B-cell lymphoma.


Journal

Journal of cancer research and clinical oncology
ISSN: 1432-1335
Titre abrégé: J Cancer Res Clin Oncol
Pays: Germany
ID NLM: 7902060

Informations de publication

Date de publication:
Mar 2021
Historique:
received: 25 07 2020
accepted: 28 10 2020
pubmed: 4 1 2021
medline: 25 2 2021
entrez: 3 1 2021
Statut: ppublish

Résumé

Some chemotherapy drugs have immunomodulatory effects on specific tumors. The potential of vincristine (VCR) in the R-CHOP regimen to act as both a chemotherapeutic and an immunomodulatory agent via PD-L1 in tumor cells remains unclear. In vitro screening VCR showed that the IC50 value of VCR in the DLBCL cell lines was approximately 2 nM. Western blotting and q-PCR were used to detect the expression of PD-L1. The effect of VCR combined with PD-L1 mAb was tested in a co-culture system of LY-OCI-3 cells and peripheral blood mononuclear cells and in DLBCL xenograft mouse model. Flow cytometry was used to determine the proportion of T lymphocyte subsets. The effect of the STAT3 inhibitor nifuroxazide on VCR-induced PD-L1 expression was tested in LY-OCI-3 and SU-DHL-4 cells. VCR upregulated PD-L1 protein and mRNA expression in various DLBCL cell lines. PD-L1 Ab combined with VCR significantly increased the proportion of CD8 + Granzyme B + , INF-γ + or TNF-α + CD3 + T cells. VCR + PD-L1 Ab inhibited tumor growth more effectively than VCR monotherapy, whereas PD-L1 Ab alone had no significant effect. Survival time did not differ significantly between the PD-L1 Ab group and the control group, whereas it was significantly longer in the VCR monotherapy and combination groups which showed more longer survival compared with the former. Nifuroxazide downregulated p-STAT3 and PD-L1 protein levels. VCR upregulated PD-L1 expression in DLBCL cells partially by promoting the p-STAT3; VCR combined with PD-L1 Ab activated effector T cells and increased the antitumor immune response in vitro and in vivo.

Sections du résumé

BACKGROUND BACKGROUND
Some chemotherapy drugs have immunomodulatory effects on specific tumors. The potential of vincristine (VCR) in the R-CHOP regimen to act as both a chemotherapeutic and an immunomodulatory agent via PD-L1 in tumor cells remains unclear.
METHODS METHODS
In vitro screening VCR showed that the IC50 value of VCR in the DLBCL cell lines was approximately 2 nM. Western blotting and q-PCR were used to detect the expression of PD-L1. The effect of VCR combined with PD-L1 mAb was tested in a co-culture system of LY-OCI-3 cells and peripheral blood mononuclear cells and in DLBCL xenograft mouse model. Flow cytometry was used to determine the proportion of T lymphocyte subsets. The effect of the STAT3 inhibitor nifuroxazide on VCR-induced PD-L1 expression was tested in LY-OCI-3 and SU-DHL-4 cells.
RESULTS RESULTS
VCR upregulated PD-L1 protein and mRNA expression in various DLBCL cell lines. PD-L1 Ab combined with VCR significantly increased the proportion of CD8 + Granzyme B + , INF-γ + or TNF-α + CD3 + T cells. VCR + PD-L1 Ab inhibited tumor growth more effectively than VCR monotherapy, whereas PD-L1 Ab alone had no significant effect. Survival time did not differ significantly between the PD-L1 Ab group and the control group, whereas it was significantly longer in the VCR monotherapy and combination groups which showed more longer survival compared with the former. Nifuroxazide downregulated p-STAT3 and PD-L1 protein levels.
CONCLUSIONS CONCLUSIONS
VCR upregulated PD-L1 expression in DLBCL cells partially by promoting the p-STAT3; VCR combined with PD-L1 Ab activated effector T cells and increased the antitumor immune response in vitro and in vivo.

Identifiants

pubmed: 33389078
doi: 10.1007/s00432-020-03446-w
pii: 10.1007/s00432-020-03446-w
doi:

Substances chimiques

Antineoplastic Agents, Immunological 0
B7-H1 Antigen 0
CD274 protein, human 0
Cd274 protein, mouse 0
Vincristine 5J49Q6B70F

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

691-701

Subventions

Organisme : Guangzhou Planned Project of Science and Technology
ID : 201707010279
Organisme : The Nature Science Foundation of China
ID : 81671632
Organisme : The Nature Science Foundation of China
ID : 81874169

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Auteurs

Ting Wei (T)

Department of Hematology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, Guangdong, People's Republic of China.

Manjun Li (M)

Department of Hematology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong Province, People's Republic of China.

Zhigang Zhu (Z)

Department of Geriatrics, Hematology and Oncology ward, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, Guangdong, People's Republic of China.

Huabao Xiong (H)

Institute of Immunology and Molecular Medicine, Jining Medical University, Jinan, 272067, Shandong, People's Republic of China.

Han Shen (H)

Department of Hematology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, Guangdong, People's Republic of China.

Hui Zhang (H)

Institute of Immunology and Molecular Medicine, Jining Medical University, Jinan, 272067, Shandong, People's Republic of China.

Qinghua Du (Q)

Department of Hematology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, Guangdong, People's Republic of China.

Qingshan Li (Q)

Department of Hematology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, Guangdong, People's Republic of China. eyqingshanli@scut.edu.cn.
Department of Hematology, Guangzhou Red Cross Hospital, Jinan University, No.396 TongFu Middle Road, Haizhu District, Guangzhou, 510220, Guangdong, People's Republic of China. eyqingshanli@scut.edu.cn.

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