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miR-202 Promotes Cell Apoptosis in Esophageal Squamous Cell Carcinoma by Targeting HSF2.

Abstract Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant cancers with high mortality around the world. However, the regulatory mechanism of ESCC carcinogenesis is not completely known. Here we demonstrate the novel role of miR-202 in regulating ESCC cell apoptosis. The analysis of data obtained from the GEO database showed that the expression of miR-202 is aberrantly decreased in tumor tissue from ESCC patients and cultured ESCC cell lines. After transfection with miR-202 mimic or inhibitor, the apoptotic capacity of ESCC cells was significantly increased by miR-202 overexpression but reduced by miR-202 repression. We then identified HSF2 as a direct target of miR-202 with the binding site on the 3'-UTR of HSF2 mRNA in ESCC cells. The apoptosis of ESCC cells induced by the miR-202 mimic could be repressed by HSF2 overexpression. Further studies indicated that HSF2 overexpression strongly upregulated the expression of Hsp70 at both the mRNA and protein levels. In addition, HSF2/Hsp70 suppressed ESCC cell apoptosis by preventing caspase 3 activation. In conclusion, miR-202 is a potential tumor suppressor in human ESCC and acts by regulating the apoptosis of ESCC cells by targeting HSF2, in which caspase 3 activation is involved. This might provide a novel therapeutic target for human ESCC.
PMID
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Authors

Mayor MeshTerms

Gene Targeting

Keywords
Journal Title oncology research
Publication Year Start




PMID- 28277193
OWN - NLM
STAT- MEDLINE
DA  - 20170309
DCOM- 20170316
LR  - 20170316
IS  - 1555-3906 (Electronic)
IS  - 0965-0407 (Linking)
VI  - 25
IP  - 2
DP  - 2017 Jan 26
TI  - miR-202 Promotes Cell Apoptosis in Esophageal Squamous Cell Carcinoma by
      Targeting HSF2.
PG  - 215-223
LID - 10.3727/096504016X14732772150541 [doi]
AB  - Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant
      cancers with high mortality around the world. However, the regulatory mechanism
      of ESCC carcinogenesis is not completely known. Here we demonstrate the novel
      role of miR-202 in regulating ESCC cell apoptosis. The analysis of data obtained 
      from the GEO database showed that the expression of miR-202 is aberrantly
      decreased in tumor tissue from ESCC patients and cultured ESCC cell lines. After 
      transfection with miR-202 mimic or inhibitor, the apoptotic capacity of ESCC
      cells was significantly increased by miR-202 overexpression but reduced by
      miR-202 repression. We then identified HSF2 as a direct target of miR-202 with
      the binding site on the 3'-UTR of HSF2 mRNA in ESCC cells. The apoptosis of ESCC 
      cells induced by the miR-202 mimic could be repressed by HSF2 overexpression.
      Further studies indicated that HSF2 overexpression strongly upregulated the
      expression of Hsp70 at both the mRNA and protein levels. In addition, HSF2/Hsp70 
      suppressed ESCC cell apoptosis by preventing caspase 3 activation. In conclusion,
      miR-202 is a potential tumor suppressor in human ESCC and acts by regulating the 
      apoptosis of ESCC cells by targeting HSF2, in which caspase 3 activation is
      involved. This might provide a novel therapeutic target for human ESCC.
FAU - Meng, Xiangrui
AU  - Meng X
AD  - Department of Oncology, The First Affiliated Hospital of Zhengzhou University,
      Zhengzhou, P.R. China.
FAU - Chen, Xiaoqi
AU  - Chen X
FAU - Lu, Peng
AU  - Lu P
FAU - Ma, Wang
AU  - Ma W
FAU - Yue, Dongli
AU  - Yue D
FAU - Song, Lijie
AU  - Song L
FAU - Fan, Qingxia
AU  - Fan Q
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Oncol Res
JT  - Oncology research
JID - 9208097
RN  - 0 (Heat-Shock Proteins)
RN  - 0 (MIRN202 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Transcription Factors)
RN  - 142297-91-4 (HSF2 protein, human)
RN  - Esophageal Squamous Cell Carcinoma
SB  - IM
MH  - Apoptosis/*physiology
MH  - Carcinoma, Squamous Cell/genetics/*metabolism
MH  - Cell Line, Tumor
MH  - Esophageal Neoplasms/genetics/*metabolism
MH  - *Gene Targeting/methods
MH  - Heat-Shock Proteins/*biosynthesis/genetics
MH  - Humans
MH  - MicroRNAs/*biosynthesis/genetics
MH  - Transcription Factors/*biosynthesis/genetics
EDAT- 2017/03/10 06:00
MHDA- 2017/03/17 06:00
CRDT- 2017/03/10 06:00
AID - 10.3727/096504016X14732772150541 [doi]
PST - ppublish
SO  - Oncol Res. 2017 Jan 26;25(2):215-223. doi: 10.3727/096504016X14732772150541.

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