Journal
MOLECULAR THERAPY-NUCLEIC ACIDS
Volume 18, Issue -, Pages 991-998Publisher
CELL PRESS
DOI: 10.1016/j.omtn.2019.10.029
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Funding
- Ministry of Science and Technology, Taiwan [MOST 106-NU-E-006-003-NU, MOST 106-2314-B-006-015-MY2, MOST 108-2314-B-006-004, MOST 107-2314-B-006-068-MY3]
- National Cheng Kung University
- Delta Electronics, Inc. [B107-K076]
- Laboratory Animal Center, College of Medicine, National Cheng Kung University
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Galectin-1 (Gal-1) is a pleiotropic homodimeric beta-galactoside-binding protein with a single carbohydrate recognition domain. It has been implicated in several biological processes that are important during tumor progression. Several lines of evidence have indicated that Gal-1 is involved in cancer immune escape and induces T cell apoptosis. These observations all emphasized Gal-1 as a novel target for cancer immunotherapy. Here, we developed a novel Gal-1-targeting DNA aptamer (AP-74 M-545) and demonstrated its antitumor effect by restoring immune function. AP-74 M-545 binds to Gal-1 with high affinity. AP-74 M-545 targets tumors in murine tumor models but suppresses tumor growth only in immunocompetent C57BL/6 mice, not in immunocompromised nonobese diabetic (NOD)/severe combined immunodeficiency (SCID) mice. Immunohistochemistry revealed increased CD4(+) and CD8(+) T cells in AP-74 M-545-treated tumor tissues. AP-74 M-545 suppresses T cell apoptosis by blocking the binding of Gal-1 to CD45, the main receptor and apoptosis mediator of Gal-1 on T cells. Collectively, our data suggest that the Gal-1 aptamer suppresses tumor growth by blocking the interaction between Gal-1 and CD45 to rescue T cells from apoptosis and restores T cell-mediated immunity. These results indicate that AP-74 M-545 may be a potential strategy for cancer immunotherapy.
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