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Olausson, Josefin
Publications (2 of 2) Show all publications
Karlsson, S., Olausson, J., Lundh, D., Sögård, P., Mandal, A., Holmström, K.-O., . . . Larsson, D. (2010). Vitamin D and prostate cancer: The role of membrane initiated signaling pathways in prostate cancer progression. Journal of Steroid Biochemistry and Molecular Biology, 121(1-2), 413-416
Open this publication in new window or tab >>Vitamin D and prostate cancer: The role of membrane initiated signaling pathways in prostate cancer progression
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2010 (English)In: Journal of Steroid Biochemistry and Molecular Biology, ISSN 0960-0760, E-ISSN 1879-1220, Vol. 121, no 1-2, p. 413-416Article in journal (Refereed) Published
Abstract [en]

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) has been demonstrated to mediate both genomic and non-genomic responses in prostate cancer (CaP) cells. Here, we give an overview of membrane initiated 1,25(OH)2D3 signaling in prostate cancer cell progression. The presence of PDIA3 was investigated and homologous modeling of the putative PDIA3 receptor complex was conducted. Furthermore, the cellular distribution of nVDR was analyzed. We could show that both nVDR and PDIA3 are expressed in the prostate cancer cell lines investigated. The homologous modeling of PDIA3 showed that the receptor complex exists in a trimer formation, which suggests for allosteric activity. Our findings support previous reports and suggest that 1,25(OH)2D3 is an important therapeutic agent in inhibiting prostate cancer progression. Furthermore, our data show that 1,25(OH)2D3 regulate prostate cell biology via multiple pathways and targeting specific pathways for 1,25(OH)2D3 might provide more effective therapies compared to the vitamin D therapies currently clinically tested.

Place, publisher, year, edition, pages
Elsevier, 2010
Keywords
1, 25(OH)2D3, Prostate cancer, Membrane receptors, PDIA3, nVDR, Receptor modeling
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-4528 (URN)10.1016/j.jsbmb.2010.03.083 (DOI)000280600200091 ()20398754 (PubMedID)2-s2.0-77954760891 (Scopus ID)
Available from: 2011-01-03 Created: 2011-01-03 Last updated: 2017-12-20Bibliographically approved
Hagberg, M., Holmén, J., Olausson, J., Karlsson, S., Johansson, V. & Larsson, D. (2008). Rapid activation of JNK/SAPK in LNCaP prostate cancer cells by 1α,25-dihydroxyvitamin D3 is independent of PDIA3 (1,25-MARRS). Current Topics in Steroid Research, 5, 17-24
Open this publication in new window or tab >>Rapid activation of JNK/SAPK in LNCaP prostate cancer cells by 1α,25-dihydroxyvitamin D3 is independent of PDIA3 (1,25-MARRS)
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2008 (English)In: Current Topics in Steroid Research, ISSN 0972-4788, Vol. 5, p. 17-24Article in journal (Refereed) Published
Abstract [en]

1α,25-dihydroxyvitamin D3 (1,25D3 ) is a highly potential anti-cancerous agent for prevention and treatment of prostate cancer, the most commonly diagnosed cancer type of males in western countries. A recent study by our laboratory, demonstrates that LNCaP cancer cells treated with 1,25D3, evoked dose-dependent activation of the JNK/SAPK MAPK signaling pathway within 10 minutes after hormone treatment, indicative of membrane-initiated steroid signaling (MISS) by 1,25D3. This confirms previous reports on intestinal-, chondrocyte- and osteoblast cells, where 1,25D3 operates through pharmacologically distinct nuclear-initiated mechanisms (NISS) and plasma membrane-initiated mechanisms. NISS is mediated via the vitamin D receptor (nVDR) and MISS is mediated through 1,25D3-MARRS (PDIA3, 1,25D3-membraneassociated rapid response steroid binding protein) or nVDR. The aims of the present study were to investigate the mechanisms of MISS evoked effects on alkaline phosphatase (ALP) and activation of the JNK/SAPK by 1,25D3, and the involvement of PDIA3 in 1,25D3 initiated activation of the JNK/SAPK signaling pathway. Furthermore, 1,25D3-treated LNCaP cells were transfected with siRNA against PDIA3 and phosphorylated JNK/SAPK was estimated by western analysis. Western analysis and ALP-assays demonstrated rapid activation of both JNK/SAPK as well as ALP. Silencing of PDIA3 did not affect 1,25D3 mediated activation of JNK/SAPK, suggesting that PDIA3 is not involved in the 1,25D3-initiated activation of the JNK/SAPK signaling pathway.

Place, publisher, year, edition, pages
Research Trends, 2008
Keywords
vitamin D, MAP kinase, JNK/SAPK, VDR, PDIA3, LNCaP, prostate cancer, 1α, 25(OH)2D3, siRNA, membrane initiated steroid signaling, MISS, alkaline phosphatase
National Category
Biochemistry and Molecular Biology Cancer and Oncology
Identifiers
urn:nbn:se:his:diva-2429 (URN)
Available from: 2008-12-05 Created: 2008-12-05 Last updated: 2019-07-03Bibliographically approved
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