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2016 ; 6
(ä): 25798
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Slug-upregulated miR-221 promotes breast cancer progression through suppressing
E-cadherin expression
#MMPMID27174021
Pan Y
; Li J
; Zhang Y
; Wang N
; Liang H
; Liu Y
; Zhang CY
; Zen K
; Gu H
Sci Rep
2016[May]; 6
(ä): 25798
PMID27174021
show ga
It is generally regarded that E-cadherin is downregulated during tumorigenesis
via Snail/Slug-mediated E-cadherin transcriptional reduction. However, this
transcriptional suppressive mechanism cannot explain the failure of producing
E-cadherin protein in metastatic breast cancer cells after overexpressing
E-cadherin mRNA. Here we reveal a novel mechanism that E-cadherin is
post-transcriptionally regulated by Slug-promoted miR-221, which serves as an
additional blocker for E-cadherin expression in metastatic tumor cells. Profiling
the predicted E-cadherin-targeting miRNAs in breast cancer tissues and cells
showed that miR-221 was abundantly expressed in breast tumor and metastatic
MDA-MB-231 cells and its level was significantly higher in breast tumor or
MDA-MB-231 cells than in distal non-tumor tissue and low-metastatic MCF-7 cells,
respectively. MiR-221, which level inversely correlated with E-cadherin level in
breast cancer cells, targeted E-cadherin mRNA open reading frame (ORF) and
suppressed E-cadherin protein expression. Depleting or increasing miR-221 level
in breast cancer cells induced or decreased E-cadherin protein level, leading to
suppressing or promoting tumor cell progression, respectively. Moreover, miR-221
was specifically upregulated by Slug but not Snail. TGF-? treatment enhanced Slug
activity and thus increased miR-221 level in MCF-7 cells. In summary, our results
provide the first evidence that Slug-upregulated miR-221 promotes breast cancer
progression via reducing E-cadherin expression.
|*Disease Progression
[MESH]
|Amino Acid Sequence
[MESH]
|Animals
[MESH]
|Antigens, CD
[MESH]
|Base Sequence
[MESH]
|Breast Neoplasms/*genetics/*pathology
[MESH]
|Cadherins/chemistry/*genetics/metabolism
[MESH]
|Cell Line, Tumor
[MESH]
|Cell Movement/genetics
[MESH]
|Disease Models, Animal
[MESH]
|Female
[MESH]
|Gene Expression Regulation, Neoplastic
[MESH]
|Humans
[MESH]
|Lung Neoplasms/secondary
[MESH]
|Mice, SCID
[MESH]
|MicroRNAs/genetics/*metabolism
[MESH]
|Models, Biological
[MESH]
|Neoplasm Invasiveness
[MESH]
|Neoplasm Metastasis
[MESH]
|RNA, Messenger/genetics/metabolism
[MESH]
|Snail Family Transcription Factors/*metabolism
[MESH]
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