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Exosomal transfer of tumor-associated macrophage-derived miR-21 confers cisplatin resistance in gastric cancer cells.

Abstract Cisplatin-based chemotherapy is frequently used to treat advanced gastric cancer (GC). However, the resistance often occurs with the mechanisms being not well understood. Recently, emerging evidence indicates that tumor-associated macrophages (TAMs) play an important role in chemoresistance of cancer. As the important mediators in intercellular communications, exosomes secreted by host cells mediate the exchange of genetic materials and proteins to be involved in tumor aggressiveness. The aim of the study was to investigate whether exosomes derived from TAMs mediate cisplatin resistance in gastric cancer.
PMID
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Authors

Mayor MeshTerms
Keywords

Cisplatin resistance

Exosome

Gastric cancer

Tumor-associated macrophages

miR-21

Journal Title journal of experimental & clinical cancer research : cr
Publication Year Start




PMID- 28407783
OWN - NLM
STAT- MEDLINE
DA  - 20170414
DCOM- 20170414
LR  - 20170416
IS  - 1756-9966 (Electronic)
IS  - 0392-9078 (Linking)
VI  - 36
IP  - 1
DP  - 2017 Apr 13
TI  - Exosomal transfer of tumor-associated macrophage-derived miR-21 confers cisplatin
      resistance in gastric cancer cells.
PG  - 53
LID - 10.1186/s13046-017-0528-y [doi]
AB  - BACKGROUND: Cisplatin-based chemotherapy is frequently used to treat advanced
      gastric cancer (GC). However, the resistance often occurs with the mechanisms
      being not well understood. Recently, emerging evidence indicates that
      tumor-associated macrophages (TAMs) play an important role in chemoresistance of 
      cancer. As the important mediators in intercellular communications, exosomes
      secreted by host cells mediate the exchange of genetic materials and proteins to 
      be involved in tumor aggressiveness. The aim of the study was to investigate
      whether exosomes derived from TAMs mediate cisplatin resistance in gastric
      cancer. METHODS: M2 polarized macrophages were obtained from mouse bone marrow or
      human PBMCs stimulated with IL-4 and IL-13. Exosomes isolated from M2 macrophages
      culture medium were characterized, and miRNA expression profiles of M2 derived
      exosomes (M2-exos) were analyzed using miRNA microarray. In vitro cell coculture 
      was further conducted to investigate M2-exos mediated crosstalk between TAMs and 
      tumor cells. Moreover, the in vivo experiments were performed using a
      subcutaneous transplantation tumor model in athymic nude mice. RESULTS: In this
      study, we showed that M2 polarized macrophages promoted cisplatin (DDP)
      resistance in gastric cancer cells and exosomes derived from M2 macrophages
      (M2-exos) are involved in mediating the resistance to DDP. Using miRNA profiles
      assay, we identify significantly higher levels of microRNA-21 (miR21) isomiRNAs
      in exosomes and cell lysate isolated from M2 polarized macrophage. Functional
      studies revealed that exosomal miR-21 can be directly transferred from
      macrophages to the gastric cancer cells, where it suppresses cell apoptosis and
      enhances activation of PI3K/AKT signaling pathway by down-regulation of PTEN.
      CONCLUSIONS: Our findings suggest that exosomal transfer of tumor-associated
      macrophages derived miR-21 confer DDP resistance in gastric cancer, and targeting
      exosome communication may be a promising new therapeutic strategy for gastric
      cancer patients.
FAU - Zheng, Peiming
AU  - Zheng P
AD  - Department of Clinical Laboratory, Xinhua Hospital, Shanghai Jiao Tong University
      School of Medicine, Shanghai, 200092, China.
FAU - Chen, Lei
AU  - Chen L
AD  - Department of General Surgery, Xinhua Hospital, Shanghai Jiao Tong University
      School of Medicine, Shanghai, 200092, China.
FAU - Yuan, Xiangliang
AU  - Yuan X
AD  - Department of Clinical Laboratory, Xinhua Hospital, Shanghai Jiao Tong University
      School of Medicine, Shanghai, 200092, China. [email protected]
FAU - Luo, Qin
AU  - Luo Q
AD  - Department of Clinical Laboratory, Xinhua Hospital, Shanghai Jiao Tong University
      School of Medicine, Shanghai, 200092, China.
FAU - Liu, Yi
AU  - Liu Y
AD  - Department of Clinical Laboratory, Xinhua Hospital, Shanghai Jiao Tong University
      School of Medicine, Shanghai, 200092, China.
FAU - Xie, Guohua
AU  - Xie G
AD  - Department of Clinical Laboratory, Xinhua Hospital, Shanghai Jiao Tong University
      School of Medicine, Shanghai, 200092, China.
FAU - Ma, Yanhui
AU  - Ma Y
AD  - Department of Clinical Laboratory, Xinhua Hospital, Shanghai Jiao Tong University
      School of Medicine, Shanghai, 200092, China.
FAU - Shen, Lisong
AU  - Shen L
AD  - Department of Clinical Laboratory, Xinhua Hospital, Shanghai Jiao Tong University
      School of Medicine, Shanghai, 200092, China. [email protected]
LA  - eng
PT  - Journal Article
DEP - 20170413
PL  - England
TA  - J Exp Clin Cancer Res
JT  - Journal of experimental & clinical cancer research : CR
JID - 8308647
RN  - 0 (MIRN21 microRNA, human)
RN  - 0 (MIRN21 microRNA, mouse)
RN  - 0 (MicroRNAs)
RN  - Q20Q21Q62J (Cisplatin)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Cell Line, Tumor
MH  - Cisplatin/*pharmacology
MH  - Drug Resistance, Neoplasm
MH  - Exosomes/genetics/*metabolism
MH  - Humans
MH  - Macrophages/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - MicroRNAs/genetics/*metabolism
MH  - Stomach Neoplasms/*drug therapy/genetics/*metabolism/pathology
PMC - PMC5390430
OTO - NOTNLM
OT  - Cisplatin resistance
OT  - Exosome
OT  - Gastric cancer
OT  - Tumor-associated macrophages
OT  - miR-21
EDAT- 2017/04/15 06:00
MHDA- 2017/04/15 06:01
CRDT- 2017/04/15 06:00
PHST- 2017/01/24 [received]
PHST- 2017/04/05 [accepted]
AID - 10.1186/s13046-017-0528-y [doi]
AID - 10.1186/s13046-017-0528-y [pii]
PST - epublish
SO  - J Exp Clin Cancer Res. 2017 Apr 13;36(1):53. doi: 10.1186/s13046-017-0528-y.

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