YY1 inhibits the migration and invasion of pancreatic ductal adenocarcinoma by downregulating the FER/STAT3/MMP2 signaling pathway

Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis and a high mortality rate. The transcription factor YY1 acts as an inhibitor of many types of tumors. We found that YY1 knockdown promoted the invasion and migration of PANC-1 and BxPC-3 cells; FER knockdown partially restored the promotio...

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Veröffentlicht in:Cancer letters 2019-10, Vol.463, p.37-49
Hauptverfasser: Chen, Qun, Zhang, Jing-Jing, Ge, Wan-Li, Chen, Lei, Yuan, Hao, Meng, Ling-Dong, Huang, Xu-Min, Shen, Peng, Miao, Yi, Jiang, Kui-Rong
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container_end_page 49
container_issue
container_start_page 37
container_title Cancer letters
container_volume 463
creator Chen, Qun
Zhang, Jing-Jing
Ge, Wan-Li
Chen, Lei
Yuan, Hao
Meng, Ling-Dong
Huang, Xu-Min
Shen, Peng
Miao, Yi
Jiang, Kui-Rong
description Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis and a high mortality rate. The transcription factor YY1 acts as an inhibitor of many types of tumors. We found that YY1 knockdown promoted the invasion and migration of PANC-1 and BxPC-3 cells; FER knockdown partially restored the promotion of pancreatic cancer caused by YY1 knockdown. In vivo experiments yielded the same results. According to luciferase reporter gene, electrophoretic mobility shift (EMSA) and chromatin immunoprecipitation (ChIP) assays, YY1 directly binds to the FER promoter region. Moreover, higher level FER expression results in a worse TNM stage and prognosis for patients with PDAC. Furthermore, by downregulating FER, YY1 inhibits the formation of the STAT3-MMP2 complex, thereby suppressing expression of MMP2 and ultimately inhibiting the migration and invasion of pancreatic cancer. Our study demonstrates that the YY1/FER/STAT3/MMP2 axis is associated with the progression of pancreatic cancer and may provide a new therapeutic target for the treatment of pancreatic cancer. [Display omitted] •YY1 inhibits the migration and invasion of pancreatic cancer cells.•YY1 down-regulates the expression of FER.•YY1 is directly combined with promoter region of FER.•YY1/FER/STAT3/MMP2 axis can serve as a novel therapeutic target for pancreatic cancer.
doi_str_mv 10.1016/j.canlet.2019.07.019
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The transcription factor YY1 acts as an inhibitor of many types of tumors. We found that YY1 knockdown promoted the invasion and migration of PANC-1 and BxPC-3 cells; FER knockdown partially restored the promotion of pancreatic cancer caused by YY1 knockdown. In vivo experiments yielded the same results. According to luciferase reporter gene, electrophoretic mobility shift (EMSA) and chromatin immunoprecipitation (ChIP) assays, YY1 directly binds to the FER promoter region. Moreover, higher level FER expression results in a worse TNM stage and prognosis for patients with PDAC. Furthermore, by downregulating FER, YY1 inhibits the formation of the STAT3-MMP2 complex, thereby suppressing expression of MMP2 and ultimately inhibiting the migration and invasion of pancreatic cancer. Our study demonstrates that the YY1/FER/STAT3/MMP2 axis is associated with the progression of pancreatic cancer and may provide a new therapeutic target for the treatment of pancreatic cancer. [Display omitted] •YY1 inhibits the migration and invasion of pancreatic cancer cells.•YY1 down-regulates the expression of FER.•YY1 is directly combined with promoter region of FER.•YY1/FER/STAT3/MMP2 axis can serve as a novel therapeutic target for pancreatic cancer.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2019.07.019</identifier><identifier>PMID: 31404611</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Adenocarcinoma ; Adenocarcinoma - metabolism ; Adenocarcinoma - physiopathology ; Breast cancer ; Cancer therapies ; Carcinoma, Pancreatic Ductal - metabolism ; Carcinoma, Pancreatic Ductal - physiopathology ; Cell cycle ; Cell motility ; Cell Movement - physiology ; Chromatin ; Cloning ; Down-Regulation ; Electrophoretic mobility ; Epidermal growth factor ; Fer tyrosine kinase ; Gelatinase A ; Gene expression ; Gene Expression Regulation, Neoplastic ; Humans ; Immunoprecipitation ; Kinases ; Liver cancer ; Matrix Metalloproteinase 2 - physiology ; Medical prognosis ; Neoplasm Invasiveness - physiopathology ; Ovarian cancer ; Pancreatic cancer ; PDAC ; Prognosis ; Protein-Tyrosine Kinases - metabolism ; Protein-Tyrosine Kinases - physiology ; Proteins ; Reporter gene ; Signal transduction ; Signal Transduction - physiology ; Stat3 protein ; STAT3 Transcription Factor - physiology ; Therapeutic applications ; Tumor Cells, Cultured ; Tumor suppression ; Tumors ; YinYang-1 ; YY1 protein ; YY1 Transcription Factor - physiology</subject><ispartof>Cancer letters, 2019-10, Vol.463, p.37-49</ispartof><rights>2019 The Author(s)</rights><rights>Copyright © 2019 The Author(s). 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The transcription factor YY1 acts as an inhibitor of many types of tumors. We found that YY1 knockdown promoted the invasion and migration of PANC-1 and BxPC-3 cells; FER knockdown partially restored the promotion of pancreatic cancer caused by YY1 knockdown. In vivo experiments yielded the same results. According to luciferase reporter gene, electrophoretic mobility shift (EMSA) and chromatin immunoprecipitation (ChIP) assays, YY1 directly binds to the FER promoter region. Moreover, higher level FER expression results in a worse TNM stage and prognosis for patients with PDAC. Furthermore, by downregulating FER, YY1 inhibits the formation of the STAT3-MMP2 complex, thereby suppressing expression of MMP2 and ultimately inhibiting the migration and invasion of pancreatic cancer. Our study demonstrates that the YY1/FER/STAT3/MMP2 axis is associated with the progression of pancreatic cancer and may provide a new therapeutic target for the treatment of pancreatic cancer. 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The transcription factor YY1 acts as an inhibitor of many types of tumors. We found that YY1 knockdown promoted the invasion and migration of PANC-1 and BxPC-3 cells; FER knockdown partially restored the promotion of pancreatic cancer caused by YY1 knockdown. In vivo experiments yielded the same results. According to luciferase reporter gene, electrophoretic mobility shift (EMSA) and chromatin immunoprecipitation (ChIP) assays, YY1 directly binds to the FER promoter region. Moreover, higher level FER expression results in a worse TNM stage and prognosis for patients with PDAC. Furthermore, by downregulating FER, YY1 inhibits the formation of the STAT3-MMP2 complex, thereby suppressing expression of MMP2 and ultimately inhibiting the migration and invasion of pancreatic cancer. Our study demonstrates that the YY1/FER/STAT3/MMP2 axis is associated with the progression of pancreatic cancer and may provide a new therapeutic target for the treatment of pancreatic cancer. [Display omitted] •YY1 inhibits the migration and invasion of pancreatic cancer cells.•YY1 down-regulates the expression of FER.•YY1 is directly combined with promoter region of FER.•YY1/FER/STAT3/MMP2 axis can serve as a novel therapeutic target for pancreatic cancer.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>31404611</pmid><doi>10.1016/j.canlet.2019.07.019</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record>
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subjects Adenocarcinoma
Adenocarcinoma - metabolism
Adenocarcinoma - physiopathology
Breast cancer
Cancer therapies
Carcinoma, Pancreatic Ductal - metabolism
Carcinoma, Pancreatic Ductal - physiopathology
Cell cycle
Cell motility
Cell Movement - physiology
Chromatin
Cloning
Down-Regulation
Electrophoretic mobility
Epidermal growth factor
Fer tyrosine kinase
Gelatinase A
Gene expression
Gene Expression Regulation, Neoplastic
Humans
Immunoprecipitation
Kinases
Liver cancer
Matrix Metalloproteinase 2 - physiology
Medical prognosis
Neoplasm Invasiveness - physiopathology
Ovarian cancer
Pancreatic cancer
PDAC
Prognosis
Protein-Tyrosine Kinases - metabolism
Protein-Tyrosine Kinases - physiology
Proteins
Reporter gene
Signal transduction
Signal Transduction - physiology
Stat3 protein
STAT3 Transcription Factor - physiology
Therapeutic applications
Tumor Cells, Cultured
Tumor suppression
Tumors
YinYang-1
YY1 protein
YY1 Transcription Factor - physiology
title YY1 inhibits the migration and invasion of pancreatic ductal adenocarcinoma by downregulating the FER/STAT3/MMP2 signaling pathway
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