Pretreatment of BMSCs with TZD solution decreases the proliferation rate of MCF‑7 cells by reducing FGF4 protein expression

Khoo,Boon‑Yin; Nadarajan,Kalpanah; Shim,Siang‑Yian; Miswan,Noorizan; Zang,Chuan‑Bing; Possinger,Kurt; Elstner,Elena

doi:10.3892/mmr.2016.4959

Pretreatment of BMSCs with TZD solution decreases the proliferation rate of MCF‑7 cells by reducing FGF4 protein expression

Authors:
- Boon‑Yin Khoo
- Kalpanah Nadarajan
- Siang‑Yian Shim
- Noorizan Miswan
- Chuan‑Bing Zang
- Kurt Possinger
- Elena Elstner
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Affiliations: Institute for Research in Molecular Medicine (INFORMM), Universiti Sains Malaysia, Penang 11800, Malaysia, Division of Oncology and Haematology, Charité Campus Mitte, Humboldt University of Berlin, D‑10099 Berlin, Germany
Published online on: March 2, 2016 https://doi.org/10.3892/mmr.2016.4959
Pages: 3406-3414
Copyright: © Khoo et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study aimed to investigate the effects of bone marrow‑derived mesenchymal stem cells (BMSCs) that had been pretreated with pioglitazone and/or rosiglitazone on the growth and proliferation rate of MCF‑7 cells. The adhesive interaction between the BMSCs and the MCF‑7 cancer cells revealed that the pretreatment of BMSCs with a combination of two types of thiazolidinedione drug reduced the growth and proliferation rate of the MCF‑7 cells. The proliferation rate of the MCF‑7 cells could also be reduced by the non‑adhesive interaction of the cancer cells with BMSCs pretreated with pioglitazone and/or rosiglitazone. The growth and proliferation rate reduction effects on the MCF‑7 cells may be attributed to the reduction in the protein level of fibroblast growth factor 4 (FGF4) in the conditioned medium of the pretreated BMSCs. The evidence that the low protein level of FGF4 in the conditioned medium of the pretreated BMSCs perturbed the proliferation rate of the MCF‑7 cells by reducing the levels of Ki‑67 and proliferating cell nuclear antigen transcripts in the cancer cells was also demonstrated in the present study using a FGF4‑neutralizing antibody. All the above findings demonstrate that future studies on the correlation between FGF4 and pretreated BMSCs would be beneficial.

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