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1000 Titel
  • c-Jun N-terminal kinase 2 suppresses pancreatic cancer growth and invasion and is opposed by c-Jun N-terminal kinase 1
1000 Autor/in
  1. Tian, Xiaodong |
  2. Traub, Benno |
  3. Shi, Jingwei |
  4. Huber, Nadine |
  5. Schreiner, Stefan |
  6. Chen, Guowei |
  7. Zhou, Shaoxia |
  8. Henne-Bruns, Doris |
  9. Knippschild, Uwe |
  10. Kornmann, Marko |
1000 Erscheinungsjahr 2021
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2021-02-01
1000 Erschienen in
1000 Quellenangabe
  • 29(1):73-86
1000 Copyrightjahr
  • 2021
1000 Lizenz
1000 Verlagsversion
  • https://doi.org/10.1038/s41417-020-00290-5 |
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8761571/ |
1000 Publikationsstatus
1000 Sprache der Publikation
1000 Abstract/Summary
  • The c-Jun N-terminal protein kinases (JNKs) JNK1 and JNK2 can act as either tumor suppressors or pro-oncogenic kinases in human cancers. The isoform-specific roles for JNK1 and JNK2 in human pancreatic cancer are still unclear, the question which should be addressed in this project. Human pancreatic cancer cell lines MIA PaCa-2 and PANC-1 clones were established either expressing either JNK1 or -2 shRNA in a stable manner. Basal anchorage-dependent and -independent cell growth, single-cell movement, and invasion using the Boyden chamber assay were analyzed. Xenograft growth was assessed using an orthotopic mouse model. All seven tested pancreatic cancer cell lines expressed JNKs as did human pancreatic cancer samples determined by immunohistochemistry. Pharmacological, unspecific JNK inhibition (SP600125) reduced cell growth of all cell lines but PANC-1. Especially inhibition of JNK2 resulted in overall increased oncogenic potential with increased proliferation and invasion, associated with alterations in cytoskeleton structure. Specific inhibition of JNK1 revealed opposing functions. Overall, JNK1 and JNK2 can exert different functions in human pancreatic cancer and act as counter players for tumor invasion. Specifically modulating the activity of JNKs may be of potential therapeutic interest in the future.
1000 Sacherschließung
lokal Mice [MeSH]
lokal Pancreatic Neoplasms/genetics [MeSH]
lokal Article
lokal Mitogen-Activated Protein Kinase 8/metabolism [MeSH]
lokal Phosphorylation [MeSH]
lokal Mitogen-Activated Protein Kinase 9/genetics [MeSH]
lokal Cancer genetics
lokal Humans [MeSH]
lokal Mitogen-Activated Protein Kinase 9/metabolism [MeSH]
lokal Mitogen-Activated Protein Kinase 8/genetics [MeSH]
lokal Animals [MeSH]
lokal Pancreatic cancer
1000 Liste der Beteiligten
  1. https://frl.publisso.de/adhoc/uri/VGlhbiwgWGlhb2Rvbmc=|https://orcid.org/0000-0001-8380-2268|https://frl.publisso.de/adhoc/uri/U2hpLCBKaW5nd2Vp|https://frl.publisso.de/adhoc/uri/SHViZXIsIE5hZGluZQ==|https://frl.publisso.de/adhoc/uri/U2NocmVpbmVyLCBTdGVmYW4=|https://frl.publisso.de/adhoc/uri/Q2hlbiwgR3Vvd2Vp|https://frl.publisso.de/adhoc/uri/WmhvdSwgU2hhb3hpYQ==|https://frl.publisso.de/adhoc/uri/SGVubmUtQnJ1bnMsIERvcmlz|https://frl.publisso.de/adhoc/uri/S25pcHBzY2hpbGQsIFV3ZQ==|https://orcid.org/0000-0002-9533-8711
1000 Hinweis
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1000 Erstellt am 2023-04-26T15:58:54.898+0200
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1000 Zuletzt bearbeitet Thu Oct 19 13:31:56 CEST 2023
1000 Objekt bearb. Thu Oct 19 13:31:56 CEST 2023
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