PMID- 27840923
OWN - NLM
STAT- MEDLINE
DCOM- 20170407
LR  - 20181202
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 14
IP  - 6
DP  - 2016 Dec
TI  - Identification of HLA‑A*1101‑restricted cytotoxic T lymphocyte epitopes derived 
      from epidermal growth factor pathway substrate number 8.
PG  - 4999-5006
LID - 10.3892/mmr.2016.5888 [doi]
AB  - Epidermal growth factor receptor pathway substrate 8 (EPS8) is critical in the 
      proliferation, progression and metastasis of solid and hematological types of 
      cancer, and thus constitutes an ideal target for cancer immunotherapy. The 
      present study aimed to identify human leukocyte antigen (HLA)‑A*1101‑restricted 
      cytotoxic T lymphocyte (CTL) epitopes from EPS8 and characterize their 
      immunotherapeutic efficacy in vitro. Two computer‑based algorithms were used to 
      predict native EPS8 epitopes with potential high binding affinity to the 
      HLA‑A*1101 molecule, which is the HLA‑A allele with the highest frequency in the 
      Chinese population. The peptide‑induced cytokine production from the CTLs was 
      examined using enzyme‑linked immunosorbent spot analysis. The cytotoxic effects 
      on cancer cells by CTLs primed with the identified peptides were examined using 
      flow cytometry. A total of five peptides, designated as P380, P70, P82, P30 and 
      P529, presented with high affinity towards the HLA‑A*1101 molecule. In response 
      to stimulation by these five peptides, enhanced secretion of interferon‑gamma from 
      the CTLs and increased cytolytic capabilities of the CTLs toward cancer cells 
      were noted, with the most potent effects observed from the P380 peptide. Taken 
      together, the present study identified five potential CTL epitopes from EPS8. 
      Among these, P380 presented with the highest therapeutic efficacy in vitro. These 
      peptides may benefit the development of EPS8‑based immunotherapy for the 
      treatment of HLA‑A*1101‑positive hematological malignancies.
FAU - Lu, Huifang
AU  - Lu H
AD  - Department of Hematology, Zhujiang Hospital, Southern Medical University, 
      Guangzhou, Guangdong 510280, P.R. China.
FAU - Tang, Baishan
AU  - Tang B
AD  - Department of Hematology, Zhujiang Hospital, Southern Medical University, 
      Guangzhou, Guangdong 510280, P.R. China.
FAU - He, Yanjie
AU  - He Y
AD  - Department of Hematology, Zhujiang Hospital, Southern Medical University, 
      Guangzhou, Guangdong 510280, P.R. China.
FAU - Zhou, Weijun
AU  - Zhou W
AD  - Department of Hematology, Zhujiang Hospital, Southern Medical University, 
      Guangzhou, Guangdong 510280, P.R. China.
FAU - Qiu, Jielei
AU  - Qiu J
AD  - Department of Hematology, Zhujiang Hospital, Southern Medical University, 
      Guangzhou, Guangdong 510280, P.R. China.
FAU - Li, Yuhua
AU  - Li Y
AD  - Department of Hematology, Zhujiang Hospital, Southern Medical University, 
      Guangzhou, Guangdong 510280, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20161025
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (EPS8 protein, human)
RN  - 0 (Epitopes, T-Lymphocyte)
RN  - 0 (HLA-A Antigens)
RN  - 0 (Peptides)
RN  - 0 (RNA, Small Interfering)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/chemistry/*immunology/metabolism
MH  - Cell Line, Tumor
MH  - Cytotoxicity, Immunologic
MH  - Epitope Mapping
MH  - Epitopes, T-Lymphocyte/*immunology
MH  - HLA-A Antigens/*immunology/metabolism
MH  - Humans
MH  - Interferon-gamma/metabolism
MH  - K562 Cells
MH  - Peptides/chemistry/immunology/metabolism
MH  - Phenotype
MH  - Protein Binding
MH  - RNA, Small Interfering/genetics
MH  - T-Lymphocytes, Cytotoxic/*immunology/metabolism
PMC - PMC5355652
EDAT- 2016/11/15 06:00
MHDA- 2017/04/08 06:00
PMCR- 2016/10/25
CRDT- 2016/11/15 06:00
PHST- 2015/08/30 00:00 [received]
PHST- 2016/09/12 00:00 [accepted]
PHST- 2016/11/15 06:00 [pubmed]
PHST- 2017/04/08 06:00 [medline]
PHST- 2016/11/15 06:00 [entrez]
PHST- 2016/10/25 00:00 [pmc-release]
AID - mmr-14-06-4999 [pii]
AID - 10.3892/mmr.2016.5888 [doi]
PST - ppublish
SO  - Mol Med Rep. 2016 Dec;14(6):4999-5006. doi: 10.3892/mmr.2016.5888. Epub 2016 Oct 
      25.