ERβ1 inhibits metastasis of androgen receptor-positive triple-negative breast cancer by suppressing ZEB1

Song, Wei; Tang, Lin; Xu, Yumei; Sun, Qiang; Yang, Fang; Guan, Xiaoxiang

doi:10.1186/s13046-017-0545-x

Cited by 25 publications

(27 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In breast cancer, knockdown of ZEB1 can lead to the downregulation of inflammatory cytokines related to poor prognosis including IL6 and IL8 (Katsura et al, ). ERβ1 can repress androgen receptor‐positive triple‐negative breast cancer metastasis via targeting ZEB1 (Song et al, ). ZEB1 can promote ER‐α promoter hypermethylation and induces antiestrogen resistance in breast cancer (Zhang, Zhou, et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…LncRNA NEAT1 can play a vital role in nuclear paraspeckles and regulate RNA splicing and transcription (Naganuma & Hirose, 2013). NEAT1 can affect the development of mouse mammary gland (Standaert et al, 2014). NEAT1 can serve as an oncogenic lncRNA in several cancers, including breast cancer (Choudhry et al, 2015;Guo et al, 2015;Lin et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

NEAT1 contributes to breast cancer progression through modulating miR‐448 and ZEB1

Jiang

Zhou

Sun

et al. 2018

Journal Cellular Physiology

106

View full text Add to dashboard Cite

Breast cancer is a kind of common female cancers. Increasing evidence has exhibited that lncRNAs exert a crucial role in breast cancer. So far, the mechanism of lncRNAs in breast cancer is still not well established. In our current study, we focused on the biological role of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in breast cancer. We observed that NEAT1 levels were significantly increased in human breast cancer cells including MCF-7, MDA-MB-453, MDA-MB-231, and SKBR3 cells compared to normal mammary epithelial cells MCF-10A while miR-448 was decreased. We found that downregulation of NEAT1 was able to inhibit the growth of breast cancer cells and miR-448 mimic exerted the similar function. Bioinformatics analysis and dual luciferase reporter assays confirmed the negative correlation between NEAT1 and miR-448 in vitro. In addition, ZEB1 was predicted as a novel mRNA target of miR-448. Overexpression of NEAT1 can induce breast cancer cell growth, migration, and invasion by inhibiting miR-448 and upregulating ZEB1. It was demonstrated that NEAT1 can increase ZEB1 levels while miR-448 mimic can repress ZEB1. It was speculated in our study that NEAT1 can serve as a competing endogenous lncRNA (ceRNA) to modulate ZEB1 by sponging miR-448 in breast cancer. To conclude, we uncovered that NEAT1 participated in breast cancer progression by regulating miR-448 and ZEB1. NEAT1 can be provided as a vital biomarker in breast cancer diagnosis and treatment therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

NEAT1 contributes to breast cancer progression through modulating miR‐448 and ZEB1

Jiang

Zhou

Sun

et al. 2018

Journal Cellular Physiology

106

View full text Add to dashboard Cite

show abstract

“…However, in MB-231 cells, DPN caused significant decrease in cellular invasion. This discrepancy could be due to the that fact that a recent study [ 67 ] had shown that MB-231 cells express androgen receptor (AR) and that in AR positive TNBC cells, ERβ decreases cellular invasion and migration. Another discrepancy could be due to the fact that these authors used an over-expressing ERβ construct, used FBS and phenol red containing media to determine invasion instead of using hormonal free FBS/phenol red free media.…”

Section: Discussionmentioning

confidence: 99%

Estrogen receptor-beta is a potential target for triple negative breast cancer treatment

et al. 2018

View full text Add to dashboard Cite

Triple Negative breast cancer (TNBC) is a subtype of breast cancer that lacks the expression of estrogen receptor (ER), progesterone receptor, and human epidermal growth factor receptor 2. TNBC accounts for 15-20% of all breast cancer cases but accounts for over 50% of mortality. We propose that Estrogen receptor-beta (ERβ) and IGF2 play a significant role in the pathogenesis of TNBCs, and could be important targets for future therapy.Tissue microarrays (TMAs) from over 250 TNBC patients' were analyzed for ERβ and IGF2 expression by immunohistochemistry. Expression was correlated with clinical outcomes. In addition, TNBC cell lines Caucasians (CA): MB-231/BT549 and African Americans (AAs): MB-468/HCC70/HCC1806 were used to investigate the effect of hormonal and growth factor regulation on cell proliferation.TMAs from AAs had higher expression of ERβ and IGF2 expression when compared to CA. ERβ and IGF2 were found to be upregulated in our TNBC cell lines when compared to other cell types. TNBC cells treated with ERβ agonist displayed significant increase in cell proliferation and migration when compared to controls. AA tissue samples from TNBC patients had higher expression of ERβ. African-American breast cancer TNBC tissue samples from TNBC patients have higher expression of ERβ. In addition, TNBC cell lines were also found to express high levels of ERβ. IGF2 increased transcription of ERβ in TNBC cells. Understanding the mechanisms of IGF2/ERβ axis in TNBC tumors could provide an opportunity to target this aggressive subtype of breast cancer.

show abstract

“…ERβ1 and ERβ2 (also known as ERβcx) are the best characterized isoforms in breast tissue. 26 , 27 Although ERα has been well established as an important mediator of proliferation in breast cancer, the role of ERβ remains controversial. Hartman et al 28 found that ERβ-positive breast cancer had a higher histological grade than ERβ-negative breast cancer.…”

Section: Discussionmentioning

confidence: 99%

The anticancer activity of genistein is increased in estrogen receptor beta 1-positive breast cancer cells

Jiang¹,

Fan²,

Lin³

et al. 2018

OTT

View full text Add to dashboard Cite

BackgroundMost breast cancers are estrogen dependent and were sensitive to endocrine therapy, and genistein (GEN) shows strong affinity with human oestrogen receptor beta (ERβ).PurposeThe present study aimed to investigate the anticancer activity of GEN in breast cancer cell lines that constitutively expressing ERβ1 in vitro and in vivo.MethodsMCF-7/ERβ1 and MDA-MB-231/ERβ1 cell sub-lines were established through lentiviral infection. Then, cells were treated with increasing concentrations of GEN (10−6 mol/l, 10−5 mol/l and 10−4 mol/l) for 48 h, and cell proliferation, cell cycle analyses were performed to investigate different biological characteristics of ERβ1-overexpressing cell lines. Studies in vivo were also performed to investigate the effects of dietary GEN on MCF-7/ERβ1 and MDA-MB-231/ERβ1 cells implanted mice.ResultsResults showed that compared to parental cells, GEN inhibited the proliferation ability of MCF-7/ERβ1 cells to a greater extent, especially at high concentrations. MDA-MB-231 cells were also inhibited by high doses of GEN, but the overexpressed ERβ1 did not enhance the anti-proliferative effect on MDA-MB-231 cells. ERβ1 arrested cells in G2/M phase, and GEN arrested cells in G0/G1, which led to a combinatorial effect on cell cycle blockade. Furthermore, ERβ1 increased the anti-tumour activity of dietary GEN in MCF-7/ERβ1 subcutaneous tumour models. Our data indicated that ERβ1 increased the anticancer efficacy of GEN in MCF-7 cells by affecting cell cycle transition.ConclusionAs a result, GEN could be a potential therapeutic agent for ERβ1-positive cancer.

show abstract

ERβ1 inhibits metastasis of androgen receptor-positive triple-negative breast cancer by suppressing ZEB1

Cited by 25 publications

References 34 publications

NEAT1 contributes to breast cancer progression through modulating miR‐448 and ZEB1

NEAT1 contributes to breast cancer progression through modulating miR‐448 and ZEB1

Estrogen receptor-beta is a potential target for triple negative breast cancer treatment

The anticancer activity of genistein is increased in estrogen receptor beta 1-positive breast cancer cells

Contact Info

Product

Resources

About