PMID- 28274095
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1976-9148 (Print)
IS  - 2005-4483 (Electronic)
IS  - 1976-9148 (Linking)
VI  - 25
IP  - 6
DP  - 2017 Nov 1
TI  - Sphingosylphosphorylcholine Induces Thrombospondin-1 Secretion in MCF10A Cells 
      via ERK2.
PG  - 625-633
LID - 10.4062/biomolther.2016.228 [doi]
AB  - Sphingosylphosphorylcholine (SPC) is one of the bioactive phospholipids that has 
      many cellular functions such as cell migration, adhesion, proliferation, 
      angiogenesis, and Ca(2)(+) signaling. Recent studies have reported that SPC induces 
      invasion of breast cancer cells via matrix metalloproteinase-3 (MMP-3) secretion 
      leading to WNT activation. Thrombospondin-1 (TSP-1) is a matricellular and 
      calcium-binding protein that binds to a wide variety of integrin and non-integrin 
      cell surface receptors. It regulates cell proliferation, migration, and apoptosis 
      in inflammation, angiogenesis and neoplasia. TSP-1 promotes aggressive phenotype 
      via epithelial mesenchymal transition (EMT). The relationship between SPC and 
      TSP-1 is unclear. We found SPC induced EMT leading to mesenchymal morphology, 
      decrease of E-cadherin expression and increases of N-cadherin and vimentin. SPC 
      induced secretion of thrombospondin-1 (TSP-1) during SPC-induced EMT of various 
      breast cancer cells. Gene silencing of TSP-1 suppressed SPC-induced EMT as well 
      as migration and invasion of MCF10A cells. An extracellular signal-regulated 
      kinase inhibitor, PD98059, significantly suppressed the secretion of TSP-1, 
      expressions of N-cadherin and vimentin, and decrease of E-cadherin in MCF10A 
      cells. ERK2 siRNA suppressed TSP-1 secretion and EMT. From online PROGgene V2, 
      relapse free survival is low in patients having high TSP-1 expressed breast 
      cancer. Taken together, we found that SPC induced EMT and TSP-1 secretion via 
      ERK2 signaling pathway. These results suggests that SPC-induced TSP-1 might be a 
      new target for suppression of metastasis of breast cancer cells.
FAU - Kang, June Hee
AU  - Kang JH
AD  - College of Pharmacy, Dongguk University, Seoul 10326, Republic of Korea.
FAU - Kim, Hyun Ji
AU  - Kim HJ
AD  - College of Pharmacy, Dongguk University, Seoul 10326, Republic of Korea.
FAU - Park, Mi Kyung
AU  - Park MK
AD  - College of Pharmacy, Dongguk University, Seoul 10326, Republic of Korea.
AD  - National Cancer Center, Goyang, 10408, Republic of Korea.
FAU - Lee, Chang Hoon
AU  - Lee CH
AD  - College of Pharmacy, Dongguk University, Seoul 10326, Republic of Korea.
LA  - eng
PT  - Journal Article
PL  - Korea (South)
TA  - Biomol Ther (Seoul)
JT  - Biomolecules & therapeutics
JID - 101472832
PMC - PMC5685432
OTO - NOTNLM
OT  - ERK2
OT  - Epithelial mesenchymal transition
OT  - Sphingosylphosphorylcholine
OT  - Thrombospondin-1
EDAT- 2017/03/10 06:00
MHDA- 2017/03/10 06:01
PMCR- 2017/11/01
CRDT- 2017/03/10 06:00
PHST- 2016/10/11 00:00 [received]
PHST- 2016/12/11 00:00 [revised]
PHST- 2017/01/09 00:00 [accepted]
PHST- 2017/03/10 06:00 [pubmed]
PHST- 2017/03/10 06:01 [medline]
PHST- 2017/03/10 06:00 [entrez]
PHST- 2017/11/01 00:00 [pmc-release]
AID - biomolther.2016.228 [pii]
AID - bt-25-625 [pii]
AID - 10.4062/biomolther.2016.228 [doi]
PST - ppublish
SO  - Biomol Ther (Seoul). 2017 Nov 1;25(6):625-633. doi: 10.4062/biomolther.2016.228.