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Regulation of matrix stiffness on the epithelial-mesenchymal transition of breast cancer cells under hypoxia environment.

Abstract Substrate stiffness and hypoxia are associated with tumor development and progression, respectively. However, the synergy of them on the biological behavior of human breast cancer cell is still largely unknown. This study explored how substrate stiffness regulates the cell phenotype, viability, and epithelial-mesenchymal transition (EMT) of human breast cancer cells MCF-7 under hypoxia (1% O2). TRITC-phalloidin staining showed that MCF-7 cells transformed from round to irregular polygon with stiffness increase either in normoxia or hypoxia. While being accompanied with the upward tendency from a 0.5- to a 20-kPa substrate, the percentage of cell apoptosis was significantly higher in hypoxia than that in normoxia, especially on the 20-kPa substrate. Additionally, it was hypoxia, but not normoxia, that promoted the EMT of MCF-7 by upregulating hypoxia-inducible factor-1α (HIF-1α), vimentin, Snail 1, and matrix metalloproteinase 2 (MMP 2) and 9 (MMP 9), and downregulating E-cadherin simultaneously regardless of the change of substrate stiffness. In summary, this study discovered that hypoxia and stiffer substrate (20 kPa) could synergistically induce phenotype change, apoptosis, and EMT of MCF-7 cells. Results of this study have an important significance on further exploring the synergistic effect of stiffness and hypoxia on the EMT of breast cancer cells and its molecular mechanism.
PMID
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Authors

Mayor MeshTerms
Keywords

Breast cancer cell

Epithelial-mesenchymal transition

Hypoxia

Phenotype

Substrate stiffness

Journal Title die naturwissenschaften
Publication Year Start




PMID- 28382476
OWN - NLM
STAT- MEDLINE
DA  - 20170406
DCOM- 20170412
LR  - 20170412
IS  - 1432-1904 (Electronic)
IS  - 0028-1042 (Linking)
VI  - 104
IP  - 5-6
DP  - 2017 Jun
TI  - Regulation of matrix stiffness on the epithelial-mesenchymal transition of breast
      cancer cells under hypoxia environment.
PG  - 38
LID - 10.1007/s00114-017-1461-9 [doi]
AB  - Substrate stiffness and hypoxia are associated with tumor development and
      progression, respectively. However, the synergy of them on the biological
      behavior of human breast cancer cell is still largely unknown. This study
      explored how substrate stiffness regulates the cell phenotype, viability, and
      epithelial-mesenchymal transition (EMT) of human breast cancer cells MCF-7 under 
      hypoxia (1% O2). TRITC-phalloidin staining showed that MCF-7 cells transformed
      from round to irregular polygon with stiffness increase either in normoxia or
      hypoxia. While being accompanied with the upward tendency from a 0.5- to a 20-kPa
      substrate, the percentage of cell apoptosis was significantly higher in hypoxia
      than that in normoxia, especially on the 20-kPa substrate. Additionally, it was
      hypoxia, but not normoxia, that promoted the EMT of MCF-7 by upregulating
      hypoxia-inducible factor-1alpha (HIF-1alpha), vimentin, Snail 1, and matrix
      metalloproteinase 2 (MMP 2) and 9 (MMP 9), and downregulating E-cadherin
      simultaneously regardless of the change of substrate stiffness. In summary, this 
      study discovered that hypoxia and stiffer substrate (20 kPa) could
      synergistically induce phenotype change, apoptosis, and EMT of MCF-7 cells.
      Results of this study have an important significance on further exploring the
      synergistic effect of stiffness and hypoxia on the EMT of breast cancer cells and
      its molecular mechanism.
FAU - Lv, Yonggang
AU  - Lv Y
AUID- ORCID: http://orcid.org/0000-0003-3966-8975
AD  - Key Laboratory of Biorheological Science and Technology, Ministry of Education,
      Bioengineering College, Chongqing University, Chongqing, 400044, People's
      Republic of China. [email protected]
AD  - Mechanobiology and Regenerative Medicine Laboratory, Bioengineering College,
      Chongqing University, 174 Shazheng Street, Shapingba District, Chongqing, 400044,
      People's Republic of China. [email protected]
FAU - Chen, Can
AU  - Chen C
AD  - Key Laboratory of Biorheological Science and Technology, Ministry of Education,
      Bioengineering College, Chongqing University, Chongqing, 400044, People's
      Republic of China.
AD  - Mechanobiology and Regenerative Medicine Laboratory, Bioengineering College,
      Chongqing University, 174 Shazheng Street, Shapingba District, Chongqing, 400044,
      People's Republic of China.
FAU - Zhao, Boyuan
AU  - Zhao B
AD  - Key Laboratory of Biorheological Science and Technology, Ministry of Education,
      Bioengineering College, Chongqing University, Chongqing, 400044, People's
      Republic of China.
AD  - Mechanobiology and Regenerative Medicine Laboratory, Bioengineering College,
      Chongqing University, 174 Shazheng Street, Shapingba District, Chongqing, 400044,
      People's Republic of China.
FAU - Zhang, Xiaomei
AU  - Zhang X
AD  - Key Laboratory of Biorheological Science and Technology, Ministry of Education,
      Bioengineering College, Chongqing University, Chongqing, 400044, People's
      Republic of China.
AD  - Mechanobiology and Regenerative Medicine Laboratory, Bioengineering College,
      Chongqing University, 174 Shazheng Street, Shapingba District, Chongqing, 400044,
      People's Republic of China.
LA  - eng
PT  - Journal Article
DEP - 20170405
PL  - Germany
TA  - Naturwissenschaften
JT  - Die Naturwissenschaften
JID - 0400767
SB  - IM
MH  - Apoptosis
MH  - Breast Neoplasms/genetics/*physiopathology
MH  - Cell Hypoxia/*physiology
MH  - Cell Shape
MH  - Epithelial-Mesenchymal Transition/*physiology
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - MCF-7 Cells
OTO - NOTNLM
OT  - Breast cancer cell
OT  - Epithelial-mesenchymal transition
OT  - Hypoxia
OT  - Phenotype
OT  - Substrate stiffness
EDAT- 2017/04/07 06:00
MHDA- 2017/04/13 06:00
CRDT- 2017/04/07 06:00
PHST- 2017/02/03 [received]
PHST- 2017/03/25 [accepted]
PHST- 2017/03/21 [revised]
AID - 10.1007/s00114-017-1461-9 [doi]
AID - 10.1007/s00114-017-1461-9 [pii]
PST - ppublish
SO  - Naturwissenschaften. 2017 Jun;104(5-6):38. doi: 10.1007/s00114-017-1461-9. Epub
      2017 Apr 5.

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