Interleukin-6/STAT3 signalling regulates adipocyte induced epithelial-mesenchymal transition in breast cancer cells

Abstract The tumour microenvironment is a key regulators of tumour progression through the secretion of growth factors that activate epithelial-mesenchymal transition (EMT). Induction of EMT is a key step for transition from a benign state to a metastatic tumour. Adipose tissue forms a bulk portion...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Jones Gyamfi, Yun-Hee Lee, Minseob Eom, Junjeong Choi
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2018
Materias:
R
Q
Acceso en línea:https://doaj.org/article/187b74812dc443519a146de4eba5ee15
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:187b74812dc443519a146de4eba5ee15
record_format dspace
spelling oai:doaj.org-article:187b74812dc443519a146de4eba5ee152021-12-02T15:08:00ZInterleukin-6/STAT3 signalling regulates adipocyte induced epithelial-mesenchymal transition in breast cancer cells10.1038/s41598-018-27184-92045-2322https://doaj.org/article/187b74812dc443519a146de4eba5ee152018-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-27184-9https://doaj.org/toc/2045-2322Abstract The tumour microenvironment is a key regulators of tumour progression through the secretion of growth factors that activate epithelial-mesenchymal transition (EMT). Induction of EMT is a key step for transition from a benign state to a metastatic tumour. Adipose tissue forms a bulk portion of the breast cancer microenvironment, emerging evidence indicates the potential for adipocytes to influence tumour progression through the secretion of adipokines that can induce EMT. The molecular mechanisms underlying how adipocytes enhance breast cancer progression is largely unknown. We hypothesized that paracrine signalling by adipocytes can activate EMT and results in increased migration and invasion characteristics of breast cancer cells. We found that IL-6 secreted by adipocytes induce EMT in breast cancer cells. The effect of IL-6 expression on EMT is mediated through activation of the signal transducer and activated of transcription 3 (STAT3). Blocking of IL-6 signalling in breast cancer cells and adipocytes, decreased proliferation, migration and invasion capabilities and altered the expression of genes regulating EMT. Together, our results suggest that matured human adipocytes can enhance the aggressive behaviour of breast cancer cells and induce an EMT-phenotype through paracrine IL-6/STAT3 signalling.Jones GyamfiYun-Hee LeeMinseob EomJunjeong ChoiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-13 (2018)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Jones Gyamfi
Yun-Hee Lee
Minseob Eom
Junjeong Choi
Interleukin-6/STAT3 signalling regulates adipocyte induced epithelial-mesenchymal transition in breast cancer cells
description Abstract The tumour microenvironment is a key regulators of tumour progression through the secretion of growth factors that activate epithelial-mesenchymal transition (EMT). Induction of EMT is a key step for transition from a benign state to a metastatic tumour. Adipose tissue forms a bulk portion of the breast cancer microenvironment, emerging evidence indicates the potential for adipocytes to influence tumour progression through the secretion of adipokines that can induce EMT. The molecular mechanisms underlying how adipocytes enhance breast cancer progression is largely unknown. We hypothesized that paracrine signalling by adipocytes can activate EMT and results in increased migration and invasion characteristics of breast cancer cells. We found that IL-6 secreted by adipocytes induce EMT in breast cancer cells. The effect of IL-6 expression on EMT is mediated through activation of the signal transducer and activated of transcription 3 (STAT3). Blocking of IL-6 signalling in breast cancer cells and adipocytes, decreased proliferation, migration and invasion capabilities and altered the expression of genes regulating EMT. Together, our results suggest that matured human adipocytes can enhance the aggressive behaviour of breast cancer cells and induce an EMT-phenotype through paracrine IL-6/STAT3 signalling.
format article
author Jones Gyamfi
Yun-Hee Lee
Minseob Eom
Junjeong Choi
author_facet Jones Gyamfi
Yun-Hee Lee
Minseob Eom
Junjeong Choi
author_sort Jones Gyamfi
title Interleukin-6/STAT3 signalling regulates adipocyte induced epithelial-mesenchymal transition in breast cancer cells
title_short Interleukin-6/STAT3 signalling regulates adipocyte induced epithelial-mesenchymal transition in breast cancer cells
title_full Interleukin-6/STAT3 signalling regulates adipocyte induced epithelial-mesenchymal transition in breast cancer cells
title_fullStr Interleukin-6/STAT3 signalling regulates adipocyte induced epithelial-mesenchymal transition in breast cancer cells
title_full_unstemmed Interleukin-6/STAT3 signalling regulates adipocyte induced epithelial-mesenchymal transition in breast cancer cells
title_sort interleukin-6/stat3 signalling regulates adipocyte induced epithelial-mesenchymal transition in breast cancer cells
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/187b74812dc443519a146de4eba5ee15
work_keys_str_mv AT jonesgyamfi interleukin6stat3signallingregulatesadipocyteinducedepithelialmesenchymaltransitioninbreastcancercells
AT yunheelee interleukin6stat3signallingregulatesadipocyteinducedepithelialmesenchymaltransitioninbreastcancercells
AT minseobeom interleukin6stat3signallingregulatesadipocyteinducedepithelialmesenchymaltransitioninbreastcancercells
AT junjeongchoi interleukin6stat3signallingregulatesadipocyteinducedepithelialmesenchymaltransitioninbreastcancercells
_version_ 1718388301750075392