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2017 ; 40
(2
): 303-310
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Role of metadherin in estrogen-regulated gene expression
#MMPMID28627585
Li Y
; Gonzalez Bosquet J
; Yang S
; Thiel KW
; Zhang Y
; Liu H
; Leslie KK
; Meng X
Int J Mol Med
2017[Aug]; 40
(2
): 303-310
PMID28627585
show ga
The disruption of estrogen signaling is widely associated with the development of
breast, endometrial and ovarian cancers. As a multifunctional mediator of
carcinogenesis, metadherin (MTDH)/astrocyte elevated gene-1 (AEG-1)
overexpression has been associated with numerous types of cancer, with reported
roles in tumor initiation, proliferation, invasion, metastasis and
chemoresistance. At the molecular level, MTDH has been shown to interact with
proteins that drive tumorigenesis, including nuclear factor-?B (NF-?B),
promyelocytic leukaemia zinc finger (PLZF), BRCA2- and CDKN1A
(p21Cip1/Waf-1/mda-6)-interacting protein ? (BCCIP?) and staphylococcal nuclease
and tudor domain containing 1 (SND1). Through the analysis of the Cancer Genome
Atlas (TCGA) datasets for estrogen receptor (ER)-positive endometrial and breast
cancers, we found that over 25% of all gene expression correlated with MTDH.
Using Affymetrix microarrays, we characterized the differences in gene expression
between estrogen-treated parental and MTDH-deficient endometrial and breast
cancer cells. We also explored a possible interaction between MTDH and ER by
immunoprecipitation, and found that MTDH and ER associated in both breast and
endometrial cancer cells in response to estrogen. Reciprocal
co-immunoprecipitation analysis demonstrated that acute estrogen stimulation
promoted the interaction of MTDH with ER in the nucleus. These data, to the best
of our knowledge, provide the first evidence that MTDH and ER? interact in the
nucleus with estrogen treatment to regulate gene expression.
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