Platelets promote invasion and induce epithelial to mesenchymal transition in ovarian cancer cells by TGF-β signaling pathway

To test whether platelets could increase invasion potential and initiate EMT in ovarian cancer cells via a TGF-β signaling pathway. Blood samples were collected in 69 patients with ovarian cancer, 16 patients with benign ovarian tumor and 64 healthy donors. SK-OV-3 and OVCAR-3 ovarian cancer cells w...

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Veröffentlicht in:	Gynecologic oncology Jg. 153; H. 3; S. 639 - 650
Hauptverfasser:	Guo, Yi, Cui, Wei, Pei, Yuqing, Xu, Danfei
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States Elsevier Inc 01.06.2019
Schlagworte:	A83–01 Adult Animals Blood Platelets Cadherins - genetics Cadherins - metabolism Cell Line, Tumor Cell Movement - drug effects Coculture Techniques Epithelial to mesenchymal transition Epithelial-Mesenchymal Transition - genetics Female Fibronectins - genetics Gene Expression Healthy Volunteers Humans Matrix Metalloproteinase 2 - genetics Matrix Metalloproteinase 2 - metabolism Mice Middle Aged Neoplasm Invasiveness Neoplasm Transplantation Ovarian cancer Ovarian Neoplasms - blood Ovarian Neoplasms - pathology Platelet Platelet Count Pyrazoles - pharmacology Receptor, Transforming Growth Factor-beta Type I - antagonists & inhibitors Signal Transduction Smad Proteins - metabolism Snail Family Transcription Factors - genetics TGF-β Thiosemicarbazones - pharmacology Transforming Growth Factor beta - blood Transforming Growth Factor beta - metabolism Up-Regulation Vimentin - genetics Epithelial to mesenchymal transition TGF-β Platelet A83–01 Ovarian cancer
ISSN:	0090-8258, 1095-6859, 1095-6859
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Abstract	To test whether platelets could increase invasion potential and initiate EMT in ovarian cancer cells via a TGF-β signaling pathway. Blood samples were collected in 69 patients with ovarian cancer, 16 patients with benign ovarian tumor and 64 healthy donors. SK-OV-3 and OVCAR-3 ovarian cancer cells were treated with platelets. Transwell assays were used to analyze the invasive capacity, and EMT was assessed by microarray analysis, quantitative real-time PCR (qPCR) and Western blotting. Activation of TGF-β pathway was examined by ELISA and Western blotting. TGF-β type I receptor (TβR I) inhibitor A83-01 was used to confirm the role of TGF-β pathway in vitro and in vivo. Clinical data showed ovarian cancer patients with elevated platelet counts had a higher incidence of advanced stages. Treatment with platelets increased the invasive properties of both cell lines. Mesenchymal markers (snail family transcriptional repressor-1, vimentin, neural cadherin, fibronectin-1 and matrix metalloproteinase-2) were up-regulated in platelet-treated cells, while the epithelial marker (epithelial cadherin) was down-regulated. Higher TGF-β level was observed in patients with elevated platelet counts when compared to the subjects. Higher levels of TGF-β were also found in culture medium treated with platelets, and cells treated with platelets also showed increased phosphorylation of Smad2. TβR I inhibitor A83–01 reversed the EMT-like alterations and inhibited platelet-induced invasion in vitro and in vivo. Platelet increased invasion potential and induced EMT in ovarian cancer cells in a TGF-β dependent pathway. Platelet-derived TGF-β may be useful as a new target treatment for ovarian cancer. •Ovarian cancer patients with elevated platelets showed higher incidence of metastasis.•Platelets increase invasive ability and induce EMT in ovarian cancer cells.•Serum TGF-β level was higher in ovarian cancer patients with elevated platelet.•TGF-β/Smad pathway was activated in platelet-treated ovarian cancer cells.•TGF-β type I receptor inhibitor A83-01 abolished platelets-induced invasion and EMT in vitro and in vivo.
AbstractList	To test whether platelets could increase invasion potential and initiate EMT in ovarian cancer cells via a TGF-β signaling pathway.OBJECTIVETo test whether platelets could increase invasion potential and initiate EMT in ovarian cancer cells via a TGF-β signaling pathway.Blood samples were collected in 69 patients with ovarian cancer, 16 patients with benign ovarian tumor and 64 healthy donors. SK-OV-3 and OVCAR-3 ovarian cancer cells were treated with platelets. Transwell assays were used to analyze the invasive capacity, and EMT was assessed by microarray analysis, quantitative real-time PCR (qPCR) and Western blotting. Activation of TGF-β pathway was examined by ELISA and Western blotting. TGF-β type I receptor (TβR I) inhibitor A83-01 was used to confirm the role of TGF-β pathway in vitro and in vivo.METHODSBlood samples were collected in 69 patients with ovarian cancer, 16 patients with benign ovarian tumor and 64 healthy donors. SK-OV-3 and OVCAR-3 ovarian cancer cells were treated with platelets. Transwell assays were used to analyze the invasive capacity, and EMT was assessed by microarray analysis, quantitative real-time PCR (qPCR) and Western blotting. Activation of TGF-β pathway was examined by ELISA and Western blotting. TGF-β type I receptor (TβR I) inhibitor A83-01 was used to confirm the role of TGF-β pathway in vitro and in vivo.Clinical data showed ovarian cancer patients with elevated platelet counts had a higher incidence of advanced stages. Treatment with platelets increased the invasive properties of both cell lines. Mesenchymal markers (snail family transcriptional repressor-1, vimentin, neural cadherin, fibronectin-1 and matrix metalloproteinase-2) were up-regulated in platelet-treated cells, while the epithelial marker (epithelial cadherin) was down-regulated. Higher TGF-β level was observed in patients with elevated platelet counts when compared to the subjects. Higher levels of TGF-β were also found in culture medium treated with platelets, and cells treated with platelets also showed increased phosphorylation of Smad2. TβR I inhibitor A83-01 reversed the EMT-like alterations and inhibited platelet-induced invasion in vitro and in vivo.RESULTSClinical data showed ovarian cancer patients with elevated platelet counts had a higher incidence of advanced stages. Treatment with platelets increased the invasive properties of both cell lines. Mesenchymal markers (snail family transcriptional repressor-1, vimentin, neural cadherin, fibronectin-1 and matrix metalloproteinase-2) were up-regulated in platelet-treated cells, while the epithelial marker (epithelial cadherin) was down-regulated. Higher TGF-β level was observed in patients with elevated platelet counts when compared to the subjects. Higher levels of TGF-β were also found in culture medium treated with platelets, and cells treated with platelets also showed increased phosphorylation of Smad2. TβR I inhibitor A83-01 reversed the EMT-like alterations and inhibited platelet-induced invasion in vitro and in vivo.Platelet increased invasion potential and induced EMT in ovarian cancer cells in a TGF-β dependent pathway. Platelet-derived TGF-β may be useful as a new target treatment for ovarian cancer.CONCLUSIONPlatelet increased invasion potential and induced EMT in ovarian cancer cells in a TGF-β dependent pathway. Platelet-derived TGF-β may be useful as a new target treatment for ovarian cancer. To test whether platelets could increase invasion potential and initiate EMT in ovarian cancer cells via a TGF-β signaling pathway. Blood samples were collected in 69 patients with ovarian cancer, 16 patients with benign ovarian tumor and 64 healthy donors. SK-OV-3 and OVCAR-3 ovarian cancer cells were treated with platelets. Transwell assays were used to analyze the invasive capacity, and EMT was assessed by microarray analysis, quantitative real-time PCR (qPCR) and Western blotting. Activation of TGF-β pathway was examined by ELISA and Western blotting. TGF-β type I receptor (TβR I) inhibitor A83-01 was used to confirm the role of TGF-β pathway in vitro and in vivo. Clinical data showed ovarian cancer patients with elevated platelet counts had a higher incidence of advanced stages. Treatment with platelets increased the invasive properties of both cell lines. Mesenchymal markers (snail family transcriptional repressor-1, vimentin, neural cadherin, fibronectin-1 and matrix metalloproteinase-2) were up-regulated in platelet-treated cells, while the epithelial marker (epithelial cadherin) was down-regulated. Higher TGF-β level was observed in patients with elevated platelet counts when compared to the subjects. Higher levels of TGF-β were also found in culture medium treated with platelets, and cells treated with platelets also showed increased phosphorylation of Smad2. TβR I inhibitor A83–01 reversed the EMT-like alterations and inhibited platelet-induced invasion in vitro and in vivo. Platelet increased invasion potential and induced EMT in ovarian cancer cells in a TGF-β dependent pathway. Platelet-derived TGF-β may be useful as a new target treatment for ovarian cancer. •Ovarian cancer patients with elevated platelets showed higher incidence of metastasis.•Platelets increase invasive ability and induce EMT in ovarian cancer cells.•Serum TGF-β level was higher in ovarian cancer patients with elevated platelet.•TGF-β/Smad pathway was activated in platelet-treated ovarian cancer cells.•TGF-β type I receptor inhibitor A83-01 abolished platelets-induced invasion and EMT in vitro and in vivo. To test whether platelets could increase invasion potential and initiate EMT in ovarian cancer cells via a TGF-β signaling pathway. Blood samples were collected in 69 patients with ovarian cancer, 16 patients with benign ovarian tumor and 64 healthy donors. SK-OV-3 and OVCAR-3 ovarian cancer cells were treated with platelets. Transwell assays were used to analyze the invasive capacity, and EMT was assessed by microarray analysis, quantitative real-time PCR (qPCR) and Western blotting. Activation of TGF-β pathway was examined by ELISA and Western blotting. TGF-β type I receptor (TβR I) inhibitor A83-01 was used to confirm the role of TGF-β pathway in vitro and in vivo. Clinical data showed ovarian cancer patients with elevated platelet counts had a higher incidence of advanced stages. Treatment with platelets increased the invasive properties of both cell lines. Mesenchymal markers (snail family transcriptional repressor-1, vimentin, neural cadherin, fibronectin-1 and matrix metalloproteinase-2) were up-regulated in platelet-treated cells, while the epithelial marker (epithelial cadherin) was down-regulated. Higher TGF-β level was observed in patients with elevated platelet counts when compared to the subjects. Higher levels of TGF-β were also found in culture medium treated with platelets, and cells treated with platelets also showed increased phosphorylation of Smad2. TβR I inhibitor A83-01 reversed the EMT-like alterations and inhibited platelet-induced invasion in vitro and in vivo. Platelet increased invasion potential and induced EMT in ovarian cancer cells in a TGF-β dependent pathway. Platelet-derived TGF-β may be useful as a new target treatment for ovarian cancer.
Author	Cui, Wei Pei, Yuqing Xu, Danfei Guo, Yi
Author_xml	– sequence: 1 givenname: Yi surname: Guo fullname: Guo, Yi – sequence: 2 givenname: Wei orcidid: 0000-0003-4445-6846 surname: Cui fullname: Cui, Wei email: wendycuiwei@sina.cn, 962077959@qq.com – sequence: 3 givenname: Yuqing surname: Pei fullname: Pei, Yuqing – sequence: 4 givenname: Danfei surname: Xu fullname: Xu, Danfei
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Keywords	Epithelial to mesenchymal transition TGF-β Platelet A83–01 Ovarian cancer
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Snippet	To test whether platelets could increase invasion potential and initiate EMT in ovarian cancer cells via a TGF-β signaling pathway. Blood samples were... To test whether platelets could increase invasion potential and initiate EMT in ovarian cancer cells via a TGF-β signaling pathway.OBJECTIVETo test whether...
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SubjectTerms	A83–01 Adult Animals Blood Platelets Cadherins - genetics Cadherins - metabolism Cell Line, Tumor Cell Movement - drug effects Coculture Techniques Epithelial to mesenchymal transition Epithelial-Mesenchymal Transition - genetics Female Fibronectins - genetics Gene Expression Healthy Volunteers Humans Matrix Metalloproteinase 2 - genetics Matrix Metalloproteinase 2 - metabolism Mice Middle Aged Neoplasm Invasiveness Neoplasm Transplantation Ovarian cancer Ovarian Neoplasms - blood Ovarian Neoplasms - pathology Platelet Platelet Count Pyrazoles - pharmacology Receptor, Transforming Growth Factor-beta Type I - antagonists & inhibitors Signal Transduction Smad Proteins - metabolism Snail Family Transcription Factors - genetics TGF-β Thiosemicarbazones - pharmacology Transforming Growth Factor beta - blood Transforming Growth Factor beta - metabolism Up-Regulation Vimentin - genetics
Title	Platelets promote invasion and induce epithelial to mesenchymal transition in ovarian cancer cells by TGF-β signaling pathway
URI	https://www.clinicalkey.com/#!/content/1-s2.0-S0090825819301362 https://dx.doi.org/10.1016/j.ygyno.2019.02.026 https://www.ncbi.nlm.nih.gov/pubmed/30928020 https://www.proquest.com/docview/2201718509
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