Epithelial‑to‑mesenchymal transition markers are differentially expressed in epithelial cancer cell lines after everolimus treatment
- Bryan Ôrtero Perez Gonçalves
- Warne Pedro de Andrade
- Letícia da Conceição Braga
- Sílvia Ligório Fialho
- Luciana Maria Silva
Affiliations: Cellular Biology, Research and Development Department, Ezequiel Dias Foundation, Belo Horizonte, Minas Gerais 30510‑010, Brazil, Hematology and Oncology Nucleus, Grupo Oncoclinicas, Belo Horizonte, Minas Gerais 30140001, Brazil, Pharmaceutical Research and Development, Ezequiel Dias Foundation, Belo Horizonte, Minas Gerais 30510‑010, Brazil
- Published online on: August 25, 2020 https://doi.org/10.3892/ol.2020.12019
Copyright: © Perez Gonçalves
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
The epithelial‑to‑mesenchymal transition (EMT) is a phenomenon during which cancer epithelial cells undergo changes in plasticity and lose cell‑cell adhesion with consequent remodeling of the extracellular matrix and development of mesenchymal characteristics. Long non‑coding RNAs (lncRNAs) have been described as EMT modulation markers, becoming a promising target in the development of new therapies for cancer. The present study aimed to investigate the role of everolimus at 100 nM as inductor of the EMT phenomenon in cell lines derived from human breast (BT‑549), colorectal (RKO‑AS45‑1) and ovary (TOV‑21G) cancer. The integrity of cellular junctions was monitored using an in vitro model of epithelial resistance. The results demonstrated that the EMT genes ZEB1, TWIST1 and TGFB1 were differentially expressed in cells treated with everolimus compared with in untreated cells. lncRNA HOTAIR was upregulated post‑treatment only in BT‑549 cells compared with in untreated cells. After treatment with everolimus, the intensity of fluorescence of P‑cadherin decreased, and that of fibronectin increased in RKO‑AS45‑1 and TOV‑21G cells compared with control cells. The transepithelial electrical resistance at the RKO‑AS45‑1 monolayer treated with everolimus started to decrease at 48 h. The changes in the gene expression and epithelial resistance may confirm the role of everolimus in EMT.