PMID- 19628018
OWN - NLM
STAT- MEDLINE
DCOM- 20100111
LR  - 20091027
IS  - 1872-8057 (Electronic)
IS  - 0303-7207 (Linking)
VI  - 314
IP  - 1
DP  - 2010 Jan 15
TI  - Identification and characterization of the hypoxia-responsive element in human 
      stanniocalcin-1 gene.
PG  - 118-27
LID - 10.1016/j.mce.2009.07.007 [doi]
AB  - In this study, we aimed to identify the hypoxia-inducible factor-1 (HIF-1) 
      binding motif in human STC1 gene promoter and to characterize the associated gene 
      transactivation mechanism. Using normoxic human nasopharyngeal cancer cells 
      (CNE2), we manipulated the stability of HIF-1 alpha protein by overexpressing 
      HIF-1 alpha or the silencing of prolyl hydroxylase-2 (PHD2), to illustrate HIF-1 
      activation of STC1 promoter-driven luciferase activity. Subsequently luciferase 
      activities of the deletion and mutated STC1 promoter constructs were investigated 
      in HIF-1 overexpressed cells. The data revealed the presence of an authentic HRE 
      motif in STC1 gene. This result was further supported by the chromatin 
      immunoprecipitation (ChIP) assay. Using a similar experimental treatment, 
      however, had no significant effect on the expression level of STC1 mRNA and 
      protein. Moreover the activation of STC1 expression can be restored by the 
      silencing of "factor inhibiting HIF-1" (FIH-1) in either HIF-1 overexpressed or 
      PHD2 silenced cells. The data implied that the HIF-1-mediated STC1 gene 
      expression required the recruitment of p300. This presumption was confirmed by 
      the use of p300 inhibitor, chetomin and HIF-1 alpha/p300 re-ChIP assay. 
      Collectively our data provide the first evidence to show that STC1 is a 
      FIH-inhibited gene with a functional HRE motif located at the upstream region 
      between -2322/-2335. The data support the need for further investigation to 
      reveal if STC1 can be used as a novel tumor marker for HIF-1 induction and for 
      the monitoring of anti-angiogenic therapy.
FAU - Law, A Y S
AU  - Law AY
AD  - Department of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong, 
      Hong Kong.
FAU - Ching, L Y
AU  - Ching LY
FAU - Lai, K P
AU  - Lai KP
FAU - Wong, Chris K C
AU  - Wong CK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090721
PL  - Ireland
TA  - Mol Cell Endocrinol
JT  - Molecular and cellular endocrinology
JID - 7500844
RN  - 0 (Glycoproteins)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (RNA, Small Interfering)
RN  - 76687-96-2 (teleocalcin)
RN  - EC 2.3.1.48 (p300-CBP Transcription Factors)
SB  - IM
MH  - Base Sequence
MH  - Cell Hypoxia/*physiology
MH  - Cell Line, Tumor
MH  - Glycoproteins/*genetics/metabolism
MH  - Humans
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/genetics/*metabolism
MH  - Molecular Sequence Data
MH  - Mutagenesis, Site-Directed
MH  - *Promoter Regions, Genetic
MH  - RNA, Small Interfering/genetics/metabolism
MH  - *Response Elements
MH  - Transcriptional Activation
MH  - p300-CBP Transcription Factors/metabolism
EDAT- 2009/07/25 09:00
MHDA- 2010/01/12 06:00
CRDT- 2009/07/25 09:00
PHST- 2009/04/23 00:00 [received]
PHST- 2009/07/09 00:00 [revised]
PHST- 2009/07/10 00:00 [accepted]
PHST- 2009/07/25 09:00 [entrez]
PHST- 2009/07/25 09:00 [pubmed]
PHST- 2010/01/12 06:00 [medline]
AID - S0303-7207(09)00365-7 [pii]
AID - 10.1016/j.mce.2009.07.007 [doi]
PST - ppublish
SO  - Mol Cell Endocrinol. 2010 Jan 15;314(1):118-27. doi: 10.1016/j.mce.2009.07.007. 
      Epub 2009 Jul 21.