Pretražite po imenu i prezimenu autora, mentora, urednika, prevoditelja

Napredna pretraga

Pregled bibliografske jedinice broj: 740064

Interactions of Hedgehog-Gli and estrogen receptor signaling pathways in breast cancer cells


Levanat, Sonja; Trnski, Diana; Uzarevic, Zvonimir; Ozretic, Petar; Musani, Vesna; Sabol, Maja
Interactions of Hedgehog-Gli and estrogen receptor signaling pathways in breast cancer cells // European Journal of cancer / Elsevier (ur.).
Amsterdam: EACR, 2014. str. S118-S118 (poster, međunarodna recenzija, sažetak, znanstveni)


CROSBI ID: 740064 Za ispravke kontaktirajte CROSBI podršku putem web obrasca

Naslov
Interactions of Hedgehog-Gli and estrogen receptor signaling pathways in breast cancer cells

Autori
Levanat, Sonja ; Trnski, Diana ; Uzarevic, Zvonimir ; Ozretic, Petar ; Musani, Vesna ; Sabol, Maja

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
European Journal of cancer / Elsevier - Amsterdam : EACR, 2014, S118-S118

Skup
23rd Biennial Congress of the European Association for Cancer Research

Mjesto i datum
Munich, Njemačka, 05.-08.07.2014

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
Interactions ; Hedgehog-Gli ; estrogen receptor signaling pathways ; breast cancer cells
(Interactions ; Hedgehog-Gli and estrogen receptor signaling pathways ; breast cancer cells)

Sažetak
Introduction Hedgehog-Gli (Hh-Gli) signaling pathway is one of the new molecular targets found upregulated in breast tumors. Estrogen receptor alpha (ERα) signaling has a key role in the development of hormone-dependent breast cancer. The aim of this study is to determine the possible combined effects of Hh-Gli pathway inhibitor cyclopamine with ER inhibitor tamoxifen in breast cancer therapy, and to establish a potential interactions between Hh-Gli and ER signaling in breast cancer. Materials and Methods ER-positive MCF-7 and ER-negative SkBr-3 breast cancer cell lines were used. Drug treatments and Competition experiments were with: cyclopamine 0.5-7.5 μM (Toronto Research Chemicals) and tamoxifen 1-10 μM (Toronto Research Chemicals). MTT and cell migration assays were used. Gene expression studies with : cyclopamine (2.5 μM), Shh protein (3 ng/ml), tamoxifen (1 μM for MCF-7 or 5 µM for SkBr-3), β-estradiol (5 nM, Sigma) or cyclopamine + tamoxifen and Transfection with GLI1 and PTCH1 silencing (Life Technologies) in MCF cells were performed, and QRT-PCR with primers for ERα, c-MYC, RPLP0, PTCH1, SMO, GLI1, SHH, andSUFU.Immunofluorescent staining, Immunoprecipitation and Western blot were performed with primary antibodies: anti-Hh (Santa Cruz, sc-9024), anti-ERα (Santa Cruz, sc-8002), anti-Ptch1 (Santa Cruz, sc-6147), anti-Gli1 (Santa Cruz, sc-20687) and Actin (Santa Cruz, sc-1616). Confocal images were examined using the Manders coefficient plugin of the ImageJ software (v 1.45e). Dynabeads Protein G (Life Technologies) were coated with anti-ERα antibody and cell lysates were immunoprecipitated as per manufacturer’s instructions. Results and Discussion ER-positive cells show decreased viability after treatment with cyclopamine, a Hh-Gli pathway inhibitor, as well as after tamoxifen (an ERα inhibitor) treatment. Simultaneous treatment with cyclopamine and tamoxifen on the other hand, causes short-term survival of cells, and only longer treatment decreases cell proliferation. The survival effect is strongest 48 hours after simultaneous treatment with both inhibitors, and we found upregulated Hh-Gli signaling under these conditions. In addition to promoting survival, the combination of these two drugs promotes cell migration and longer treatment decreases Hh-Gli signaling as well as ERα levels. We also show a direct interaction between Shh and ERα. Shh protein is able to bind and activate ERα independently of the canonical Hh-Gli signaling pathway. Conclusion The mechanism which is responsible for the increased viability of ER-positive cell line after combined treatment with cyclopamine and tamoxifen is not clear. Although Hh-Gli signaling seems to be a good potential target for breast cancer therapy, combined treatment of cyclopamine and tamoxifen may induce an opposite effect, providing cells with short-term survival.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti



POVEZANOST RADA


Projekti:
098-0982464-2461 - Prijenos signala u tumorima: Hh-Gli put, interakcije i potencijalne terapije (Levanat, Sonja, MZOS ) ( POIROT)

Ustanove:
Institut "Ruđer Bošković", Zagreb,
Fakultet za odgojne i obrazovne znanosti, Osijek

Profili:

Avatar Url Vesna Musani (autor)

Avatar Url Petar Ozretić (autor)

Avatar Url Diana Trnski (autor)

Avatar Url Maja Sabol (autor)

Avatar Url Sonja Levanat (autor)

Avatar Url Zvonimir Užarević (autor)


Citiraj ovu publikaciju

Levanat, Sonja; Trnski, Diana; Uzarevic, Zvonimir; Ozretic, Petar; Musani, Vesna; Sabol, Maja
Interactions of Hedgehog-Gli and estrogen receptor signaling pathways in breast cancer cells // European Journal of cancer / Elsevier (ur.).
Amsterdam: EACR, 2014. str. S118-S118 (poster, međunarodna recenzija, sažetak, znanstveni)
Levanat, S., Trnski, D., Uzarevic, Z., Ozretic, P., Musani, V. & Sabol, M. (2014) Interactions of Hedgehog-Gli and estrogen receptor signaling pathways in breast cancer cells. U: Elsevier (ur.)European Journal of cancer.
@article{article, year = {2014}, pages = {S118-S118}, keywords = {Interactions, Hedgehog-Gli, estrogen receptor signaling pathways, breast cancer cells}, title = {Interactions of Hedgehog-Gli and estrogen receptor signaling pathways in breast cancer cells}, keyword = {Interactions, Hedgehog-Gli, estrogen receptor signaling pathways, breast cancer cells}, publisher = {EACR}, publisherplace = {Munich, Njema\v{c}ka} }
@article{article, year = {2014}, pages = {S118-S118}, keywords = {Interactions, Hedgehog-Gli and estrogen receptor signaling pathways, breast cancer cells}, title = {Interactions of Hedgehog-Gli and estrogen receptor signaling pathways in breast cancer cells}, keyword = {Interactions, Hedgehog-Gli and estrogen receptor signaling pathways, breast cancer cells}, publisher = {EACR}, publisherplace = {Munich, Njema\v{c}ka} }




Contrast
Increase Font
Decrease Font
Dyslexic Font