MiR‐34a modulates ErbB2 in breast cancer

Wang, Yilin; Zhang, Xiaolong; Zou, Chao; Kung, Hsiang‐Fu; Lin, Marie Chia‐mi; Dress, Andreas; Wardle, Fiona C.; Jiang, Bing-Hua; Lai, Lihui

doi:10.1002/cbin.10700

Cited by 26 publications

(14 citation statements)

References 44 publications

(51 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, high miR-26a expression is associated with decreased expression of known cell cycle regulatory targets, including Cyclin E1, EZH2, and Cdk1, and positive clinical outcomes in patients with metastatic breast cancer taking tamoxifen [ 96 ]. Overexpression of the tumor suppressor miR-34a has also been reported to suppress ErbB2 expression and breast cancer cell growth and invasion [ 97 ]. Given the oncogenic function of ErbB2 in acquired tamoxifen resistance, miR-34a expression may be a prognostic target to predict tamoxifen responsiveness in ER + breast cancer patients.…”

Section: Mirnas and Drug Resistancementioning

confidence: 99%

microRNA Regulation in Estrogen Receptor-Positive Breast Cancer and Endocrine Therapy

Howard

Yang

2018

Biol Proced Online

View full text Add to dashboard Cite

As de novo and acquired resistance to standard first line endocrine therapies is a growing clinical challenge for estrogen receptor-positive (ER+) breast cancer patients, understanding the mechanisms of resistance is critical to develop novel therapeutic strategies to prevent therapeutic resistance and improve patient outcomes. The widespread post-transcriptional regulatory role that microRNAs (miRNAs) can have on various oncogenic pathways has been well-documented. In particular, several miRNAs are reported to suppress ERα expression via direct binding with the 3’ UTR of ESR1 mRNA, which can confer resistance to estrogen/ERα-targeted therapies. In turn, estrogen/ERα activation can modulate miRNA expression, which may contribute to ER+ breast carcinogenesis. Given the reported oncogenic and tumor suppressor functions of miRNAs in ER+ breast cancer, the targeted regulation of specific miRNAs is emerging as a promising strategy to treat ER+ breast cancer and significantly improve patient responsiveness to endocrine therapies. In this review, we highlight the major miRNA-ER regulatory mechanisms in context with ER+ breast carcinogenesis, as well as the critical miRNAs that contribute to endocrine therapy resistance or sensitivity. Collectively, this comprehensive review of the current literature sheds light on the clinical applications and challenges associated with miRNA regulatory mechanisms and novel miRNA targets that may have translational value as potential therapeutics for the treatment of ER+ breast cancer.

show abstract

Section: Mirnas and Drug Resistancementioning

confidence: 99%

microRNA Regulation in Estrogen Receptor-Positive Breast Cancer and Endocrine Therapy

Howard

Yang

2018

Biol Proced Online

View full text Add to dashboard Cite

show abstract

“…Fu et al found miR‐124 enhanced radiotherapy resistance in HER2‐positive breast cancer cells. Recently, Wang et al proved that miR‐24a could negatively regulate HER2 levels in breast cancer. Furthermore, miR‐495 has been reported abnormally expressed in many cancers and participated in cell proliferation, migration, and invasion .…”

Section: Discussionmentioning

confidence: 99%

Lnc RNA SNHG20 participated in proliferation, invasion, and migration of breast cancer cells via miR‐495

Guan

Zhang

Chen

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

To explore the mechanism of lnc SNHG20 in the regulation of proliferation, invasion, and migration of breast cancer cells. mRNA levels of SNHG20, miR-495, and HER2 were detected by qRT-PCR. Protein level of HER2 was measured by Western blot. Cell proliferation, invasion, and migration were detected by CCK-8 assay, Boyden chamber assay, and Transwell assay. The combination between SNHG20 and miR-495 was confirmed by RNA pull down assay. The combination between miR-495 and HER2 was confirmed by luciferase report assays. We also established breast cancer-bearing mice model and analyzed tumor volumes. Our data showed SNHG20 expression was significantly upregulated, miR-495 expression was significantly downregulated, and HER2 expression was significantly upregulated in breast cancer tissues and cell lines. Besides, SNHG20 promoted the proliferation, invasion, and migration of breast cancer cells. We also found SNHG20 negatively regulated miR-495, and miR-495 could negatively regulate HER2. Moreover, we discovered that SNHG20 regulated HER2 via miR-495. SNHG20 regulated proliferation, invasion, and migration of breast cancer cells via miR-495/HER2. Finally, we confirmed the mechanism of SNHG20 in the regulation of proliferation, invasion, and migration in breast cancer-bearing mice model. SNHG20 regulates HER2 via miR-495 to promote proliferation, invasion, and migration of breast cancer cells.

show abstract

“…Interestingly, in the stratification analysis, we observed that the protective effect of rs11471161 in breast cancer was significant in ERBB2‐negative status (Table ). As the inhibition or knockdown of ERBB2 reduces proliferation and induces the apoptosis of breast cancer cells, it is reasonable to speculate that rs11471161 might interact with AC104135.3 and eventually influence breast cancer risk through ERBB2 signaling. In addition, we observed that breast cancer risk was also reduced in ER/PR‐positive women, women with a younger age at menarche, women with early age at first child‐birth, and premenopausal women.…”

Section: Discussionmentioning

confidence: 99%

Potentially functional variants in lncRNAs are associated with breast cancer risk in a Chinese population

Jiang

Chen

et al. 2017

Molecular Carcinogenesis

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) participate in the development of breast cancer. Genetic variants in lncRNAs may be involved in their abnormal expressions and associated with cancer risk. In the present study, we performed RNA sequencing on five paired breast cancer tumor and adjacent non-cancerous tissues to obtain differentially expressed lncRNAs. We systematically selected potential regulatory variants of these lncRNAs and investigated the associations between these variants and breast cancer susceptibility in 1486 breast cancer cases and 1519 cancer-free controls in a Chinese population. Eleven lncRNAs were significantly differentially expressed between breast cancer tumor and normal tissues (false discovery rate (FDR) ≤0.05 and fold-change ≥2), including two known lncRNAs HOTAIR and UCA1. We subsequently genotyped 20 variants located on these lncRNAs and identified two variants (rs11471161 in AC104135.3 and rs3751232 in RP11-1060J15.4) associated with breast cancer risk. Logistic regression analysis indicated that the variant allele of rs11471161 was significantly associated with a decreased breast cancer risk (additive model: OR = 0.84, 95%CI = 0.74-0.94, P = 0.004), while the variant allele of rs3751232 showed an increased risk of breast cancer (additive model: OR = 1.20, 95%CI = 1.02-1.40, P = 0.027). Further co-expression analysis indicated that AC104135.3 associated with ERBB2, which promotes the development and progression of breast cancer through overexpression. Together, these results suggest that genetic variants rs11471161 and rs3751232 in AC104135.3, and RP11-1060J15.4, respectively, may influence the susceptibility to breast cancer in the Chinese population. Further functional evaluations and larger studies are warranted to validate these findings.

show abstract

MiR‐34a modulates ErbB2 in breast cancer

Cited by 26 publications

References 44 publications

microRNA Regulation in Estrogen Receptor-Positive Breast Cancer and Endocrine Therapy

microRNA Regulation in Estrogen Receptor-Positive Breast Cancer and Endocrine Therapy

Lnc RNA SNHG20 participated in proliferation, invasion, and migration of breast cancer cells via miR‐495

Potentially functional variants in lncRNAs are associated with breast cancer risk in a Chinese population

Contact Info

Product

Resources

About