dc.contributor.author | Koutsilieris, M. | en |
dc.contributor.author | Reyes-Moreno, C. | en |
dc.contributor.author | Choki, I. | en |
dc.contributor.author | Sourla, A. | en |
dc.contributor.author | Doillon, C. | en |
dc.contributor.author | Pavlidis, Nicholas | en |
dc.creator | Koutsilieris, M. | en |
dc.creator | Reyes-Moreno, C. | en |
dc.creator | Choki, I. | en |
dc.creator | Sourla, A. | en |
dc.creator | Doillon, C. | en |
dc.creator | Pavlidis, Nicholas | en |
dc.date.accessioned | 2018-06-22T09:53:51Z | |
dc.date.available | 2018-06-22T09:53:51Z | |
dc.date.issued | 1999 | |
dc.identifier.uri | https://gnosis.library.ucy.ac.cy/handle/7/42054 | |
dc.description.abstract | One-third of women with breast cancer will develop bone metastases and eventually die from disease progression at these sites. Therefore, we analyzed the ability of human MG-63 osteoblast-like cells (MG-63 cells), MG- 63 conditioned media (MG-63 CM), insulin-like growth factor I (IGF-I), and transforming growth factor beta 1 (TGF-β1) to alter the effects of adriamycin on cell cycle and apoptosis of estrogen receptor negative (ER-) MDA-MB-231 and positive (ER+) MCF-7 breast cancer cells, using cell count, trypan blue exclusion, flow cytometry, detection of DNA fragmentation by simple agarose gel, and the terminal deoxynudeotidyl transferase (TdT)- mediated nick end-labeling method for apoptosis (TUNEL assay). Adriamycin arrested MCF-7 and MDA-MB-231 cells at G2/M phase in the cell cycle and inhibited cell growth. In addition, addamycin arrested the MCF-7 cells at G1/G0 phase and induced apoptosis of MDA-MB-231 cells. Exogenous IGF-I partially neutralized the adriamycin cytotoxicity/cytostasis of cancer cells. MG-63 CM and TGF-β1 partially neutralized the adriamycin cytotoxicity of MDA-MB-231 cells but enhanced adriamycin blockade of MCF-7 cells at G1/G0 phase. MG-63 osteoblast-like cells inhibited growth of MCF-7 cells while promoting growth and rescued MDA-MB-231 cells from adriamycin apoptosis in a collagen coculture system. These data suggest that osteoblast-derived growth factors can alter the chemotherapy response of breast cancer cells. Conceivably, host tissue (bone)-tumor cell interactions can modify the clinical response to chemotherapy in patients with advanced breast cancer. | en |
dc.language.iso | eng | en |
dc.source | Molecular Medicine | en |
dc.subject | Article | en |
dc.subject | Female | en |
dc.subject | Antineoplastic agents | en |
dc.subject | Cancer chemotherapy | en |
dc.subject | Doxorubicin | en |
dc.subject | Human | en |
dc.subject | Humans | en |
dc.subject | Breast cancer | en |
dc.subject | Breast neoplasms | en |
dc.subject | Controlled study | en |
dc.subject | Drug response | en |
dc.subject | Priority journal | en |
dc.subject | Dose-response relationship | en |
dc.subject | Drug | en |
dc.subject | Bone metastasis | en |
dc.subject | Cell division | en |
dc.subject | Receptors | en |
dc.subject | Estrogen receptor | en |
dc.subject | Cancer cell | en |
dc.subject | Human cell | en |
dc.subject | Apoptosis | en |
dc.subject | Flow cytometry | en |
dc.subject | Estrogen | en |
dc.subject | Growth inhibition | en |
dc.subject | Cell count | en |
dc.subject | Cell culture techniques | en |
dc.subject | Cell cycle | en |
dc.subject | Cell interaction | en |
dc.subject | Collagen | en |
dc.subject | Cultured | en |
dc.subject | Cytostasis | en |
dc.subject | Dna fragment | en |
dc.subject | Drug cytotoxicity | en |
dc.subject | Growth substances | en |
dc.subject | Insulin-like growth factor i | en |
dc.subject | Osteoblast | en |
dc.subject | Osteoblasts | en |
dc.subject | Osteosarcoma cell | en |
dc.subject | Somatomedin c | en |
dc.subject | Transforming growth factor beta | en |
dc.subject | Transforming growth factor beta1 | en |
dc.subject | Tumor cells | en |
dc.title | Chemotherapy cytotoxicity of human MCF-7 and MDA-MB 231 breast cancer cells is altered by osteoblast-derived growth factors | en |
dc.type | info:eu-repo/semantics/article | |
dc.description.volume | 5 | |
dc.description.issue | 2 | |
dc.description.startingpage | 86 | |
dc.description.endingpage | 97 | |
dc.author.faculty | Ιατρική Σχολή / Medical School | |
dc.author.department | Ιατρική Σχολή / Medical School | |
dc.type.uhtype | Article | en |
dc.contributor.orcid | Pavlidis, Nicholas [0000-0002-2195-9961] | |
dc.gnosis.orcid | 0000-0002-2195-9961 | |