PMID- 23437226
OWN - NLM
STAT- MEDLINE
DCOM- 20130910
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 2
DP  - 2013
TI  - Identification of special AT-rich sequence binding protein 1 as a novel tumor 
      antigen recognized by CD8+ T cells: implication for cancer immunotherapy.
PG  - e56730
LID - 10.1371/journal.pone.0056730 [doi]
LID - e56730
AB  - BACKGROUND: A large number of human tumor-associated antigens that are recognized 
      by CD8(+) T cells in a human leukocyte antigen class I (HLA-I)-restricted fashion 
      have been identified. Special AT-rich sequence binding protein 1 (SATB1) is 
      highly expressed in many types of human cancers as part of their neoplastic 
      phenotype, and up-regulation of SATB1 expression is essential for tumor survival 
      and metastasis, thus this protein may serve as a rational target for cancer 
      vaccines. METHODOLOGY/PRINCIPAL FINDINGS: Twelve SATB1-derived peptides were 
      predicted by an immuno-informatics approach based on the HLA-A*02 binding motif. 
      These peptides were examined for their ability to induce peptide-specific T cell 
      responses in peripheral blood mononuclear cells (PBMCs) obtained from HLA-A*02(+) 
      healthy donors and/or HLA-A*02(+) cancer patients. The recognition of HLA-A*02(+) 
      SATB1-expressing cancer cells was also tested. Among the twelve SATB1-derived 
      peptides, SATB1(565-574) frequently induced peptide-specific T cell responses in 
      PBMCs from both healthy donors and cancer patients. Importantly, 
      SATB1(565-574)-specific T cells recognized and killed HLA-A*02(+) SATB1(+) cancer 
      cells in an HLA-I-restricted manner. CONCLUSIONS/SIGNIFICANCE: We have identified 
      a novel HLA-A*02-restricted SATB1-derived peptide epitope recognized by CD8(+) T 
      cells, which, in turn, recognizes and kills HLA-A*02(+) SATB1(+) tumor cells. The 
      SATB1-derived epitope identified may be used as a diagnostic marker as well as an 
      immune target for development of cancer vaccines.
FAU - Wang, Mingjun
AU  - Wang M
AD  - Center for Inflammation and Epigenetics, The Methodist Hospital Research 
      Institute, Houston, Texas, USA.
FAU - Yin, Bingnan
AU  - Yin B
FAU - Matsueda, Satoko
AU  - Matsueda S
FAU - Deng, Lijuan
AU  - Deng L
FAU - Li, Ying
AU  - Li Y
FAU - Zhao, Wei
AU  - Zhao W
FAU - Zou, Jia
AU  - Zou J
FAU - Li, Qingtian
AU  - Li Q
FAU - Loo, Christopher
AU  - Loo C
FAU - Wang, Rong-Fu
AU  - Wang RF
FAU - Wang, Helen Y
AU  - Wang HY
LA  - eng
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20130221
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antigens, Neoplasm)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Cancer Vaccines)
RN  - 0 (Epitopes)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Matrix Attachment Region Binding Proteins)
RN  - 0 (Peptides)
RN  - 0 (SATB1 protein, human)
SB  - IM
MH  - Antigens, Neoplasm/*genetics
MH  - Biomarkers, Tumor/genetics/immunology
MH  - CD8-Positive T-Lymphocytes/immunology
MH  - Cancer Vaccines/genetics/immunology
MH  - Cell Line, Tumor
MH  - Epitopes/genetics/immunology
MH  - Gene Expression Regulation, Neoplastic/immunology
MH  - Histocompatibility Antigens Class I/genetics/*immunology
MH  - Humans
MH  - Immunotherapy
MH  - Matrix Attachment Region Binding Proteins/*genetics/immunology
MH  - Neoplasms/genetics/*immunology/*therapy
MH  - Peptides/genetics/immunology
PMC - PMC3578933
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/02/26 06:00
MHDA- 2013/09/11 06:00
PMCR- 2013/02/21
CRDT- 2013/02/26 06:00
PHST- 2012/10/26 00:00 [received]
PHST- 2013/01/14 00:00 [accepted]
PHST- 2013/02/26 06:00 [entrez]
PHST- 2013/02/26 06:00 [pubmed]
PHST- 2013/09/11 06:00 [medline]
PHST- 2013/02/21 00:00 [pmc-release]
AID - PONE-D-12-33037 [pii]
AID - 10.1371/journal.pone.0056730 [doi]
PST - ppublish
SO  - PLoS One. 2013;8(2):e56730. doi: 10.1371/journal.pone.0056730. Epub 2013 Feb 21.