Glypican-3-specific cytotoxic T lymphocytes induced by human leucocyte antigen-A*0201-restricted peptide effectively kill hepatocellular carcinoma cells  in vitro

Zeng, Jiangzheng; Liu, Yu; Huang, Fen; Zhou, He; Sun, Huizhen; Lu, Yao; Lei, Junhua; Luo, Rong

doi:10.1016/j.apjtm.2017.10.013

Cited by 2 publications

(2 citation statements)

References 31 publications

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“…Then, we further confirmed that these candidate peptides had good binding power and stability to HLA-A2 molecules through T2 cell binding assay. While the T2 cell binding assay has been widely used in similar studies, 24 , 25 , 45 it should be noted that it does not directly confirm peptide-HLA stability. Therefore, we conduct several complementary assays to address this limitation.…”

Section: Discussionmentioning

confidence: 99%

Prediction and identification of HLA-A*0201-restricted epitopes from cancer testis antigen CT23

Zeng,

Nong,

Zou

et al. 2023

Human Vaccines & Immunotherapeutics

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Cancer-testis antigen CT23 is a class of tumor-associated antigens (TAA) characterized by restricted expression in male germ cells and a variety of tumor tissues. Numerous studies have shown that CT23 is closely related to tumor cell viability, proliferation, metastasis and invasion. CT23 is immunogenic and can cause specific immune response in tumor patients. Therefore, it is considered to be one of the best target antigens for designing therapeutic tumor vaccines and T-cell-mediated tumor immunotherapy. In this study, we initially obtained seven HLA-A*0201-restricted CT23 epitope candidate peptides through the T cell epitope prediction program. Subsequently, a T2 cell binding assay revealed the potential binding of all candidate peptides with HLA-A2 molecules. Notably, peptide P7 (ALLVLCYSI) exhibited the highest affinity, as evidenced by a fluorescence index (FI) of 2.19. Dendritic cells (DCs) loaded with CT23 candidate peptide can stimulate CD8 + T cell activation and proliferation, and compared with other candidate peptides, candidate peptide P7 is superior. The cytotoxic T lymphocytes (CTLs) stimulated by the peptide P7 had killing effect on tumor cells (HLA-A*0201 + , CT23 + ), but no killing effect on tumor cells (HLA-A*0201 − , CT23 + ). The CTLs induced by the peptide P7 also had a specific killing effect on T2 cells bearing the peptide P7. In summary, our findings suggest that the CT23 peptide P7 (ALLVLCYSI) can induce immune responses and holds potential for tumor-specific CTL therapy.

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Section: Discussionmentioning

confidence: 99%

Prediction and identification of HLA-A*0201-restricted epitopes from cancer testis antigen CT23

Zeng,

Nong,

Zou

et al. 2023

Human Vaccines & Immunotherapeutics

View full text Add to dashboard Cite

show abstract

“…Numerous studies have revealed that tumor-specific CTLs possess favorable cytotoxicity towards various types of cancer cell; in the presence of glypican-3 (GPC3), GPC3-specific CTLs diminish hepatocellular carcinoma cells ( 37 ), and melanoma-associated antigen 3 (MAGE-3)-specific CTLs inhibits the proliferation of bladder cancer cells and the growth of tumor xenografts in nude mice ( 38 ). Furthermore, mucin 1-specific CTLs show the potential to treat several cancer types, such as pancreatic cancer, melanoma, and colon cancer ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

OCT4 and SOX2 Specific Cytotoxic T Cells Exhibit Not Only Good Efficiency but Also Synergize PD-1 Inhibitor (Nivolumab) in Treating Breast Cancer Stem-Like Cells and Drug-Resistant Breast Cancer Mice

Peng

Chang

et al. 2022

Front. Oncol.

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PurposeThis study aimed to investigate the effect of OCT4&SOX2 specific cytotoxic T lymphocytes (CTLs) plus programmed cell death protein-1 (PD-1) inhibitor (nivolumab) on treating breast cancer stem-like cells (BCSCs) in vitro and drug-resistance breast cancer (DRBC) mice in vivo.MethodsIn total, 160 breast cancer patients were enrolled following the immunofluorescence assay to detect tumor OCT4 and SOX2 expressions. CD154-activated B cells were co-cultured with CD8+ T cells (from breast cancer patients) in the presence of OCT4&SOX2 peptides, CMV pp65 peptides (negative control), and no peptides (normal control). MCF7-BCSCs were constructed by drug-resistance experiment and sphere-formation assay, then DRBC mice were constructed by planting MCF7-BCSCs. Subsequently, different doses of OCT4&SOX2 CTLs and PD-1 inhibitor (nivolumab) were used to treat MCF7-BCSCs and DRBC mice.ResultsOCT4 and SOX2 correlated with poor differentiation, more advanced stage, and worse prognosis in breast cancer patients. In vitro, OCT4&SOX2 CTLs with effector-target ratio (ETR) 5:1, 10:1 and 20:1 presented with increased cytotoxic activity compared to CMV pp65 CTLs with ETR 20:1 (negative control) and Control CTLs with ETR 20:1 (normal control) on killing MCF7-BCSCs. Besides, PD-1 inhibitor (nivolumab) improved the cytotoxic activity of OCT4&SOX2 CTLs against MCF7-BCSCs in a dose-dependent manner. In vivo, OCT4&SOX2 CTLs plus PD-1 inhibitor (nivolumab) decreased tumor volume and tumor weight while increased tumor apoptosis rate compared to OCT4&SOX2 CTLs alone, PD-1 inhibitor (nivolumab) alone, and control.ConclusionOCT4&SOX2 CTLs exhibit good efficiency and synergize PD-1 inhibitor (nivolumab) in treating BCSCs and DRBC.

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Glypican-3-specific cytotoxic T lymphocytes induced by human leucocyte antigen-A*0201-restricted peptide effectively kill hepatocellular carcinoma cells in vitro

Abstract: The GPC3 522-530 peptide contains antigen-determinant and its specific CTLs can effectively kill HCC in a HLA-A2-restricted and peptide-dependent manner. Our findings suggest that this peptide may be valuable for development of therapeutic vaccine.

Cited by 2 publications

References 31 publications

Prediction and identification of HLA-A*0201-restricted epitopes from cancer testis antigen CT23

Prediction and identification of HLA-A*0201-restricted epitopes from cancer testis antigen CT23

OCT4 and SOX2 Specific Cytotoxic T Cells Exhibit Not Only Good Efficiency but Also Synergize PD-1 Inhibitor (Nivolumab) in Treating Breast Cancer Stem-Like Cells and Drug-Resistant Breast Cancer Mice

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