ArticleHuman vaccines & immunotherapeutics2015
MC32 tumor cells acquire Ag-specific CTL resistance through the loss of CEA in a colon cancer model.
Article in Human vaccines & immunotherapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 10 citations in OpenAlex.
- Isoginkgetin derivative IP2 enhances the adaptive immune response against tumor antigens.Communications biology · 2021Article
- Regulation of the translation activity of antigen-specific mRNA is responsible for antigen loss and tumor immune escape in a HER2-expressing tumor model.Scientific reports · 2019Article
- PLAC1-specific TCR-engineered T cells mediate antigen-specific antitumor effects in breast cancer.Oncology letters · 2018Article
- Multi-target chimaeric VLP as a therapeutic vaccine in a model of colorectal cancer.Journal for immunotherapy of cancer · 2017Article
- DNA vaccines, electroporation and their applications in cancer treatment.Human vaccines & immunotherapeutics · 2015Review
- DNA vaccines 2014 meeting: Highlights and overview.Human vaccines & immunotherapeutics · 2015Article
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
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Abstract
We previously reported that MC32 cells resist carcinoembryonic antigen (CEA) DNA vaccination by losing their antigen presentation to Ag-specific CTLs in the context of MHC class I antigens in a colon cancer therapeutic model. In this study, we selected 2 tumor cells, MC32-S2-2 and MC32-S4-2, which have the ability to form tumors in CEA DNA vaccine-immunized mice. Wild type MC32 cells grew significantly less in CEA-immunized mice (with Ag-specific CTL lytic activity) than in control mice (with no Ag-specific CTL lytic activity). However, MC32-S2-2 and MC32-S4-2 cells grew at a similar rate in both control and CEA-immunized mice, confirming their resistant status against CEA DNA vaccination. MC32-S2-2 and MC32-S4-2 cells were not susceptible to lysis by CEA-specific CD8+ T cells. Moreover, when MC32-S2-2 and MC32-S4-2 cells were used as stimulating agents of CEA-specific immune cells for IFN-γ production, these cells failed to stimulate the induction of Ag-specific IFN-γ, suggesting a loss of tumor cell recognition by Ag-specific immune cells. However, MC32-S2-2 and MC32-S4-2 cells expressed MHC class I antigens in a manner similar to that of wild type MC32 cells. Finally, Western blot assay confirmed that in MC32-S2-2 and MC32-S4-2 cells, CEA expression remained absent but mouse CEA was expressed. Taken together, these data show that MC32 cells may also be able to achieve resistance to CEA-specific CTLs by antigen loss in this model.
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