Overexpression of microRNA-155 enhances the efficacy of dendritic cell vaccine against breast cancer.


Journal

Oncoimmunology
ISSN: 2162-4011
Titre abrégé: Oncoimmunology
Pays: United States
ID NLM: 101570526

Informations de publication

Date de publication:
2020
Historique:
received: 24 04 2019
revised: 19 11 2019
accepted: 21 11 2019
entrez: 3 3 2020
pubmed: 3 3 2020
medline: 3 3 2020
Statut: epublish

Résumé

MicroRNA 155 (miR-155) plays important roles in the regulation of the development and functions of a variety of immune cells. We previously revealed a vital role of miR-155 in regulating the function of dendritic cells (DCs) in breast cancer. miR-155 deficiency in DCs impaired their maturation, migration, cytokine production, and ability to activate T cells. In the current study, to exploit the therapeutic value of miR-155 for breast cancer, we examined the impact of overexpression of miR-155 on antitumor responses generated by DC vaccines. We boosted miR-155 expression in DCs by generating a miR-155 transgenic mouse strain (miR-155tg) or using lentivirus transduction. DCs overexpressing miR-155 exhibited enhanced functions in response to tumor antigens. Using miR-155 overexpressing DCs, we generated a DC vaccine and found that the vaccine resulted in enhanced antitumor immunity against established breast cancers in mice, demonstrated by increased effector T cells in the mice, suppressed tumor growth, and drastically reduced lung metastasis. Our current study suggests that in future DC vaccine development for breast cancer or other solid tumors, introducing forced miR155 overexpression in DCs via various approaches such as viral transduction or nanoparticle delivery, as well as including other adjuvant agents such as TLR ligands or immune stimulating cytokines, may unleash the full therapeutic potential of the DC vaccines.

Identifiants

pubmed: 32117588
doi: 10.1080/2162402X.2020.1724761
pii: 1724761
pmc: PMC7028336
doi:

Substances chimiques

Cancer Vaccines 0
MIRN155 microRNA, human 0
MicroRNAs 0
Mirn155 microRNA, mouse 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Pagination

1724761

Subventions

Organisme : NCCIH NIH HHS
ID : P01 AT003961
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA218578
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA216230
Pays : United States

Informations de copyright

© 2020 The Author(s). Published with license by Taylor & Francis Group, LLC.

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Auteurs

Johnie Hodge (J)

Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC, USA.

Fang Wang (F)

Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC, USA.
Department of Microbiology, Air Force Medical University, Xi'an, China.

Junfeng Wang (J)

Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC, USA.

Qing Liu (Q)

Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC, USA.

Fatma Saaoud (F)

Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC, USA.

Yuzhen Wang (Y)

Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC, USA.

Udai P Singh (UP)

Department of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC, USA.

Hexin Chen (H)

Department of Biological Sciences, University of South Carolina, Columbia, SC, USA.

Ming Luo (M)

Center for Diagnostics and Therapeutics, Department of Chemistry, Georgia State University, Atlanta, GA, USA.

Walden Ai (W)

Department of Biology and Environmental Health Science, Benedict College, Columbia, SC, USA.

Daping Fan (D)

Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC, USA.

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