WFRF:(Linderholm Barbro)
Sökning: WFRF:(Linderholm Barbro) > An autocrine VEGF/V...
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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 03764naa a2200373 4500 | |
| 001 | oai:DiVA.org:liu-50142 | |
| 003 | SwePub | |
| 008 | 091011s2008 | |||||||||||000 ||eng| | |
| 009 | oai:prod.swepub.kib.ki.se:117752220 | |
| 024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-501422 URI |
| 024 | 7 | a https://doi.org/10.1158/1541-7786.MCR-07-21722 DOI |
| 024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1177522202 URI |
| 040 | a (SwePub)liud (SwePub)ki | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Aesoy, R.u Department of Oncology/Pathology, Karolinska Biomics Center, Karolinska Institutet, Stockholm, Sweden4 aut |
| 245 | 1 0 | a An autocrine VEGF/VEGFR2 and p38 signaling loop confers resistance to 4-hydroxytamoxifen in MCF-7 breast cancer cells |
| 264 | 1 | c 2008 |
| 338 | a print2 rdacarrier | |
| 520 | a Tamoxifen, a partial estrogen receptor antagonist, is part of the standard treatment of both primary and advanced breast cancers. However, significant proportions of breast cancers are either de novo resistant or develop tamoxifen resistance during the course of treatment through mechanisms which have been only partly characterized. We have previously found that high vascular endothelial growth factor (VEGF) or VEGF receptor 2 (VEGFR2) expression and concomitant high p38 mitogen-activated protein kinase activity within breast cancers predict a poor outcome for tamoxifen-treated patients. Here, we have molecularly dissected how VEGF/VEGFR2 and p38 are linked, and contribute to tamoxifen resistance within breast cancer using a MCF-7 BC cell model with different 4-hydroxytamoxifen (4-OHT) responsiveness. We report that MCF-7 breast cancer cell lines with tamoxifen resistance have increased secretion of VEGF and increased signaling through VEGFR2 compared with parental MCF-7 cells. 4-OHT treatment caused the ablation of VEGF secretion in parental MCF-7 cells, whereas in the tamoxifen-resistant subline, a VEGF/ VEGFR2 signaling loop was still evident upon treatment. Increased basal levels of total and phosphorylated p38 were observed in tamoxifen-resistant cells. Pharmacologic inhibition of p38 reduced the proliferation of both tamoxifen-responsive and tamoxifen-resistant cells and showed an additive growth-inhibitory effect in combination with 4-OHT. A connection between VEGF/ VEGFR2 and p38 signaling was identified by VEGF and VEGFR2 knockdown, which equally reduced both the total and the active forms of p38 in tamoxifen-resistant cells. Taken together, our results suggest that decreased sensitivityto 4-OHT is caused by a death-protecting VEGF/VEGFR2 and p38 growth factor loop in breast cancer cells. Inhibition of these signaling pathways may be beneficial to overcome tamoxifen resistance. Copyright © 2008 American Association for Cancer Research. | |
| 653 | a MEDICINE | |
| 653 | a MEDICIN | |
| 700 | 1 | a Sanchez, B.C.u Karolinska Institutet4 aut |
| 700 | 1 | a Norum, J.H.u Karolinska Institutet4 aut |
| 700 | 1 | a Lewensohn, R.u Karolinska Institutet4 aut |
| 700 | 1 | a Viktorsson, K.u Karolinska Institutet4 aut |
| 700 | 1 | a Linderholm, Barbrou Karolinska Institutet,Östergötlands Läns Landsting,Onkologiska kliniken US4 aut |
| 710 | 2 | a Karolinska Institutetb Department of Oncology/Pathology, Karolinska Biomics Center, Karolinska Institutet, Stockholm, Sweden4 org |
| 773 | 0 | t Molecular Cancer Researchg 6:10, s. 1630-1638q 6:10<1630-1638x 1541-7786x 1557-3125 |
| 856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-50142 |
| 856 | 4 8 | u https://doi.org/10.1158/1541-7786.MCR-07-2172 |
| 856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:117752220 |
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