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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005273naa a2200505 4500
001oai:DiVA.org:umu-150769
003SwePub
008180831s2018 | |||||||||||000 ||eng|
009oai:lup.lub.lu.se:9473913f-5dc9-45d9-96a9-a80036e946b1
024a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1507692 URI
024a https://doi.org/10.1186/s10020-018-0035-42 DOI
024a https://lup.lub.lu.se/record/9473913f-5dc9-45d9-96a9-a80036e946b12 URI
040 a (SwePub)umud (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Mandel, Annau Umeå University,Umeå universitet,Institutionen för molekylärbiologi (Medicinska fakulteten)4 aut0 (Swepub:umu)anma0626
2451 0a The interplay between AR, EGF receptor and MMP-9 signaling pathways in invasive prostate cancer
264 c 2018-06-27
264 1b Springer,c 2018
338 a electronic2 rdacarrier
520 a Background: Metastatic Prostate cancer (PCa) cells have gained survival and invasive advantages. Epidermal growth factor (EGA) receptor is a receptor tyrosine kinase, which may mediate signalling to promote progression and invasion of various cancers. In this study, we uncovered the molecular mechanisms underlying the interconnection among the androgen receptor (AR), matrix metalloproteinase-9 (MMP9) and EGFR in promoting PCa progression. Methods: Immunohistochemical analysis of the tissue microarrays consisting of primary and metastatic PCa tissues was performed. The clinical importance of EGFR and its association with survivals were analyzed using three cohorts from MSKCC Prostate Oncogenome Project dataset (For primary tumors, n = 181; for metastatic tumors n = 37) and The Cancer Genome Atlas Prostate Adenocarcinoma Provisional dataset (n = 495). Targeted overexpression or inhibition of the proteins of interests was introduced into PCa cell lines. Treatment of PCa cell lines with the compounds was conducted. Immunoblot analysis was performed. Results: We showed that AR, MMP-9 and EGFR are interconnect factors, which may cooperatively promote PCa progression. Altered EGFR expression was associated with poor disease-free survival in PCa patients. Induced overexpression of AR led to an increase in the expression of EGFR, p-GSK-313 and decrease in p27 expression in PCa cell lines in the presence of androgen stimulation. Overexpression of MMP9 significantly induced EGFR expression in PCa cells. Inhibition of PIP5K1a, a lipid kinase that acts upstream of PI3K/AKT greatly reduced expressions of AR, MMP-9 and EGFR. Conclusions: Our findings also suggest that PCa cells may utilize AR, EGFR and MMP-9 pathways in androgen-dependent as well as in castration-resistant conditions. Our data suggest a new therapeutic potential to block cancer metastasis by targeting AR, EGFR and MMP-9 pathways in subsets of PCa patients.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinsk bioteknologix Medicinsk bioteknologi0 (SwePub)304012 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Medical Biotechnologyx Medical Biotechnology0 (SwePub)304012 hsv//eng
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaper0 (SwePub)3012 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicine0 (SwePub)3012 hsv//eng
653 a Prostate cancer
653 a Cancer metastasis
653 a Epidermal growth factor receptor
653 a Androgen receptor and androgen
700a Larsson, Peru Umeå University,Umeå universitet,Institutionen för molekylärbiologi (Medicinska fakulteten)4 aut
700a Sarwar, Martuzau Lund University,Lunds universitet,Experimentell cancerforskning, Malmö,Forskargrupper vid Lunds universitet,Experimental Cancer Research, Malmö,Lund University Research Groups4 aut0 (Swepub:lu)med-mzs
700a Semenas, Juliusu Umeå University,Umeå universitet,Institutionen för molekylärbiologi (Medicinska fakulteten)4 aut0 (Swepub:umu)juse0005
700a Khaja, Azharuddin Sajid Syedu Umeå University,Umeå universitet,Institutionen för molekylärbiologi (Medicinska fakulteten)4 aut
700a Persson, Jenny L.u Umeå University,Lund University,Lunds universitet,Umeå universitet,Institutionen för molekylärbiologi (Medicinska fakulteten),Experimentell cancerforskning, Malmö,Forskargrupper vid Lunds universitet,Experimental Cancer Research, Malmö,Lund University Research Groups4 aut0 (Swepub:lu)medk-jpe
710a Umeå universitetb Institutionen för molekylärbiologi (Medicinska fakulteten)4 org
773t Molecular Medicined : Springerg 24, s. 1-13q 24<1-13x 1076-1551x 1528-3658
856u https://doi.org/10.1186/s10020-018-0035-4y Fulltext
856u https://umu.diva-portal.org/smash/get/diva2:1244388/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
856u https://molmed.biomedcentral.com/track/pdf/10.1186/s10020-018-0035-4
856u http://dx.doi.org/10.1186/s10020-018-0035-4x freey FULLTEXT
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-150769
8564 8u https://doi.org/10.1186/s10020-018-0035-4
8564 8u https://lup.lub.lu.se/record/9473913f-5dc9-45d9-96a9-a80036e946b1

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