Cargando…
Hispidulin modulates epithelial-mesenchymal transition in breast cancer cells
Breast cancer is the most commonly diagnosed cancer worldwide. Despite the use of chemotherapeutic drugs, drug resistance has been observed in numerous patients with breast cancer. Epithelial-mesenchymal transition (EMT) is an important initiation step in the process of metastasis, whereby cancer ce...
Autores principales: | , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7798102/ https://www.ncbi.nlm.nih.gov/pubmed/33552273 http://dx.doi.org/10.3892/ol.2020.12416 |
_version_ | 1783634993025646592 |
---|---|
author | Kim, Hyun A. Lee, Joomin |
author_facet | Kim, Hyun A. Lee, Joomin |
author_sort | Kim, Hyun A. |
collection | PubMed |
description | Breast cancer is the most commonly diagnosed cancer worldwide. Despite the use of chemotherapeutic drugs, drug resistance has been observed in numerous patients with breast cancer. Epithelial-mesenchymal transition (EMT) is an important initiation step in the process of metastasis, whereby cancer cells move away from the original tumor site. Therefore, the discovery of new substances that suppress EMT is a promising avenue for cancer treatment. The present study investigated the effect of hispidulin, a polyphenolic flavonoid, on EMT in human breast cancer cells in vitro (MCF-7 and HCC38). The EMT-associated mRNA and protein expression levels were measured using reverse transcription-quantitative PCR or western blot analysis. Hispidulin treatment increased the expression levels of EMT-associated epithelial markers and decreased the expression levels of mesenchymal markers in both cells. Transforming growth factor-β1 (TGF-β1) treatment increased breast cancer cell viability (assessed via MTS assay) and EMT induction. However, hispidulin and TGF-β1 co-treatment increased the expression levels of E-cadherin and occludin, while downregulating vimentin expression. Additionally, hispidulin treatment inhibited TGF-β1-induced Smad2/3 signaling and cell migration in both breast cancer cell lines. Overall, the current findings suggested that hispidulin may inhibit EMT and cell migration by suppressing the Smad2/3 signaling pathway in breast cancer cells. |
format | Online Article Text |
id | pubmed-7798102 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-77981022021-02-04 Hispidulin modulates epithelial-mesenchymal transition in breast cancer cells Kim, Hyun A. Lee, Joomin Oncol Lett Articles Breast cancer is the most commonly diagnosed cancer worldwide. Despite the use of chemotherapeutic drugs, drug resistance has been observed in numerous patients with breast cancer. Epithelial-mesenchymal transition (EMT) is an important initiation step in the process of metastasis, whereby cancer cells move away from the original tumor site. Therefore, the discovery of new substances that suppress EMT is a promising avenue for cancer treatment. The present study investigated the effect of hispidulin, a polyphenolic flavonoid, on EMT in human breast cancer cells in vitro (MCF-7 and HCC38). The EMT-associated mRNA and protein expression levels were measured using reverse transcription-quantitative PCR or western blot analysis. Hispidulin treatment increased the expression levels of EMT-associated epithelial markers and decreased the expression levels of mesenchymal markers in both cells. Transforming growth factor-β1 (TGF-β1) treatment increased breast cancer cell viability (assessed via MTS assay) and EMT induction. However, hispidulin and TGF-β1 co-treatment increased the expression levels of E-cadherin and occludin, while downregulating vimentin expression. Additionally, hispidulin treatment inhibited TGF-β1-induced Smad2/3 signaling and cell migration in both breast cancer cell lines. Overall, the current findings suggested that hispidulin may inhibit EMT and cell migration by suppressing the Smad2/3 signaling pathway in breast cancer cells. D.A. Spandidos 2021-02 2020-12-31 /pmc/articles/PMC7798102/ /pubmed/33552273 http://dx.doi.org/10.3892/ol.2020.12416 Text en Copyright: © Kim et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Kim, Hyun A. Lee, Joomin Hispidulin modulates epithelial-mesenchymal transition in breast cancer cells |
title | Hispidulin modulates epithelial-mesenchymal transition in breast cancer cells |
title_full | Hispidulin modulates epithelial-mesenchymal transition in breast cancer cells |
title_fullStr | Hispidulin modulates epithelial-mesenchymal transition in breast cancer cells |
title_full_unstemmed | Hispidulin modulates epithelial-mesenchymal transition in breast cancer cells |
title_short | Hispidulin modulates epithelial-mesenchymal transition in breast cancer cells |
title_sort | hispidulin modulates epithelial-mesenchymal transition in breast cancer cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7798102/ https://www.ncbi.nlm.nih.gov/pubmed/33552273 http://dx.doi.org/10.3892/ol.2020.12416 |
work_keys_str_mv | AT kimhyuna hispidulinmodulatesepithelialmesenchymaltransitioninbreastcancercells AT leejoomin hispidulinmodulatesepithelialmesenchymaltransitioninbreastcancercells |