Neuregulin-1 induces cancer stem cell characteristics in breast cancer cell lines.

Abstract:

:In breast cancer, neuregulin-1 (NRG1) is known as a ligand for the HER3 receptor, which has no intrinsic tyrosine kinase activity. When activated by NRG1 binding, the HER3 receptor forms a heterodimer with other HER family receptors and mediates downstream signaling pathways, leading to multiple effects including growth, proliferation, decreased apoptosis, cellular migration and angiogenesis. Cancer stem cells (CSCs), a subgroup of cancer cells, are considered to have features of stem cells such as self-renewal ability and pluripotent differentiation into other types of mature cells. This study showed that NRG1 treatment induced CSC characteristics in breast cancer cell lines. Using breast cancer cell lines, MCF-7, SKBr-3 and MDA-MB 468, changes related to CSC characteristics were analyzed. Flow cytometry was used to analyze changes in CSC fractions in multiple cell lines after NRG1 treatment. Western blot analysis and immunofluorescence staining demonstrated the expression of CSC markers. To confirm that NRG1 treatment acts through the HER3 receptor, inhibition studies using small interfering RNA (siRNA) were performed. In MCF-7 and SKBr-3 cells, increases in the CSC fraction and expression of CSC markers were observed after NRG1 treatment. However, MDA-MB 468 cells showed high intrinsic expression of CSC markers and a high cellular fraction of CSCs, and in these cells, NRG1 treatment caused no significant change in CSC characteristics. Inhibition of the HER3 receptor blocked the NRG1-induced CSC characteristics, indicating that NRG1 functions through the HER3 receptor. The results imply the presence of a mechanism by which the HER receptors, activated by NRG1, contribute to the acquisition of CSC-like characteristics in some types of breast cancer.

journal_name

Oncol Rep

journal_title

Oncology reports

authors

Jeong H,Kim J,Lee Y,Seo JH,Hong SR,Kim A

doi

10.3892/or.2014.3330

subject

Has Abstract

pub_date

2014-09-01 00:00:00

pages

1218-24

issue

3

eissn

1021-335X

issn

1791-2431

journal_volume

32

pub_type

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