Knockdown of SPRY4 and SPRY4-IT1 inhibits cell growth and phosphorylation of Akt in human testicular germ cell tumours

Das, Mrinal Kumar; Furu, Kari; Evensen, Herman Sebastian Folkestad; Haugen, Øyvind Pernell; Haugen, Trine B.

dc.contributor.author	Das, Mrinal Kumar
dc.contributor.author	Furu, Kari
dc.contributor.author	Evensen, Herman Sebastian Folkestad
dc.contributor.author	Haugen, Øyvind Pernell
dc.contributor.author	Haugen, Trine B.
dc.date.accessioned	2019-02-06T09:11:14Z
dc.date.accessioned	2019-03-15T15:11:03Z
dc.date.available	2019-02-06T09:11:14Z
dc.date.available	2019-03-15T15:11:03Z
dc.date.issued	2018-02-06
dc.identifier.citation	Das M, Furu K, Evensen HSF, Haugen ØP, Haugen TB. Knockdown of SPRY4 and SPRY4-IT1 inhibits cell growth and phosphorylation of Akt in human testicular germ cell tumours. Scientific Reports. 2018;8(1):2462	en
dc.identifier.issn	2045-2322
dc.identifier.issn	2045-2322
dc.identifier.uri	https://hdl.handle.net/10642/6786
dc.description.abstract	Testicular germ cell tumour (TGCT) is the most common cancer in young men in large parts of the world, but the aetiology is mainly unknown. Genome-wide association studies have so far identified about 50 susceptibility loci associated with TGCT, including SPRY4. SPRY4 has shown tumour suppressor activity in several cancer cells, such as lung and prostate, while it was found to act as an oncogene in ovarian cancer. An intronic region within the SPRY4 gene produces a long non-coding RNA, SPRY4-IT1, which has been reported to act as an oncogene in melanoma, breast cancer, and colorectal cancer, and as a tumour suppressor in lung cancer. The roles of SPRY4 and SPRY4-IT1 in TGCT development are yet unknown. We found higher expression levels of SPRY4, both mRNA and protein, and of SPRY4-IT1 in human TGCT than in normal adult testis. Small-interfering RNA (siRNA)-mediated transient knockdown of SPRY4 and SPRY4-IT1 in two TGCT cell lines 833 K and NT2-D1 resulted in decreased cell growth, migration, and invasion. Knockdown of SPRY4 and SPRY4-IT1 also led to a significant reduction in the phosphorylation of Akt. Our findings indicate that SPRY4 and SPRY4-IT1 may act as oncogenes in TGCTs via activation of the PI3K / Akt signalling pathway.	en
dc.language.iso	en	en
dc.publisher	Nature Research	en
dc.relation.ispartofseries	Scientific Reports;Volume 8, Article number: 2462 (2018)
dc.rights	This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.	en
dc.rights.uri	http://creativecommons.org/licenses/by/4.0/
dc.subject	Cell invasions	en
dc.subject	Experimental disease models	en
dc.subject	Extracellular signalling molecules	en
dc.subject	RNA interferences	en
dc.title	Knockdown of SPRY4 and SPRY4-IT1 inhibits cell growth and phosphorylation of Akt in human testicular germ cell tumours	en
dc.type	Journal article	en
dc.type	Peer reviewed	en
dc.date.updated	2019-02-06T09:11:14Z
dc.description.version	publishedVersion	en
dc.identifier.doi	http://dx.doi.org/10.1038/s41598-018-20846-8
dc.identifier.cristin	1588586
dc.source.journal	Scientific Reports

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This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

Med mindre annet er angitt, så er denne innførselen lisensiert som This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.