Long non-coding RNA UCA1 enhances tamoxifen resistance in breast cancer cells through a miR-18a-HIF1α feedback regulatory loop

Li, Xiunan; Wu, Yumei; Liu, Aihui; Tang, Xin

doi:10.1007/s13277-016-5348-8

Cited by 101 publications

(85 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[39] Another study showed that endogenous UCA1 knockdown significantly reduced the number of invading cells, suggesting that UCA1 upregulation increased the invasiveness of BC cells by activating Wnt/β-catenin signaling pathway. [40] Li et al [41] investigated the expression level of UCA1 in acquired tamoxifen resistance in estrogen receptor (ER)-positive breast cancer cells and argued that downregulation of UCA1 could enhance the sensitivity of breast cancer cells to tamoxifen resistance directly interact with miR-143. In contrast, Lee et al [42] suggest that special AT-rich sequence binding protein 1 is the upstream regulator of UCA1 expression and depletion of UCA1 could suppress tumor growth and cell survival of breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

A three-long noncoding RNA signature as a diagnostic biomarker for differentiating between triple-negative and non-triple-negative breast cancers

2017

View full text Add to dashboard Cite

Background:Triple-negative breast cancer (TNBC) is an aggressive cancer with unfavorable outcome and it is useful to explore noninvasive biomarkers for its early diagnosis. Here, we identified differentially expressed long noncoding RNAs (lncRNAs) in blood samples of patients with TNBC to assess their diagnostic value.Methods:Differential expression of lncRNAs in plasma of patients with TNBC (n = 25) and non-TNBC (NTNBC; n = 35) and in healthy controls was compared by microarray analysis and validated by real-time PCR. lncRNA expression between plasma and BC tissues was compared using Pearson correlation test. Logit model was used to obtain a new lncRNA-based score. Receiver operating characteristic analysis was performed to assess the diagnostic value of the selected lncRNAs.Results:Microarray data showed that 41 lncRNAs were aberrantly expressed. Among these, antisense noncoding RNA in the INK4 locus (ANRIL), hypoxia inducible factor 1alpha antisense RNA-2 (HIF1A-AS2), and urothelial carcinoma-associated 1 (UCA1) were markedly upregulated in plasma of patients with TNBC compared with patients with NTNBC (P < 0.01). HIF1A-AS2 expression was positively associated with its tissue levels (r = 0.670, P < 0.01). AUC (95% CI) of ANRIL, HIF1A-AS2, and UCA1 was 0.785 (0.660–0.881), 0.739 (0.610–0.844), and 0.817 (0.696–0.905), respectively. TNBCSigLnc-3, a new score obtained using the logit model, showed excellent diagnostic performance, with AUC of 0.934 (0.839–0.982), sensitivity of 76.0%, and specificity of 97.1%.Conclusion:ANRIL, HIF1A-AS2, and UCA1 expression was significantly increased in plasma of patients with TNBC, suggesting their use as TNBC-specific diagnostic biomarkers.

show abstract

Section: Discussionmentioning

confidence: 99%

A three-long noncoding RNA signature as a diagnostic biomarker for differentiating between triple-negative and non-triple-negative breast cancers

2017

View full text Add to dashboard Cite

show abstract

“…Tamoxifen has been a mainstay chemotherapy utilized in breast cancer since its approval in the 1980s [457]. The lncRNA UCA1 has now been identified as a critical mediator of tamoxifen resistance in breast cancer by various mechanisms including sponging of miR-18a, a negative regulator of HIF1α [195], mTOR signalling [458], exosomal delivery of the lncRNA from resistant to sensitive cells [201], or via the Wnt/β-Catenin Pathway [190]. Other EMT associated lncRNAs which have been shown to affect tamoxifen sensitivity in breast cancer include MALAT-1 [99], lncRNA-ROR [459], and HOTAIR [460].…”

Section: Lncrnas Emt and Drug Resistancementioning

confidence: 99%

Long Non-Coding RNAs: Key Regulators of Epithelial-Mesenchymal Transition, Tumour Drug Resistance and Cancer Stem Cells

Heery

Finn

Cuffe

et al. 2017

Cancers

163

140

View full text Add to dashboard Cite

Epithelial mesenchymal transition (EMT), the adoption by epithelial cells of a mesenchymal-like phenotype, is a process co-opted by carcinoma cells in order to initiate invasion and metastasis. In addition, it is becoming clear that is instrumental to both the development of drug resistance by tumour cells and in the generation and maintenance of cancer stem cells. EMT is thus a pivotal process during tumour progression and poses a major barrier to the successful treatment of cancer. Non-coding RNAs (ncRNA) often utilize epigenetic programs to regulate both gene expression and chromatin structure. One type of ncRNA, called long non-coding RNAs (lncRNAs), has become increasingly recognized as being both highly dysregulated in cancer and to play a variety of different roles in tumourigenesis. Indeed, over the last few years, lncRNAs have rapidly emerged as key regulators of EMT in cancer. In this review, we discuss the lncRNAs that have been associated with the EMT process in cancer and the variety of molecular mechanisms and signalling pathways through which they regulate EMT, and finally discuss how these EMT-regulating lncRNAs impact on both anti-cancer drug resistance and the cancer stem cell phenotype.

show abstract

Section: Breast Cancermentioning

confidence: 99%

“…Tamoxifen is one of the major hormone therapies for endoplasmic reticulum positive breast cancer in clinical practice, and acquired resistance to tamoxifen remains a major obstacle in breast cancer treatment [110]. Tamoxifen treatment up-regulated expression of UCA1 in breast cancer cells through a miR-18a-HIF1a feedback loop [110]. The overexpression of UCA1 conferred tamoxifen resistance by increasing the activity of Wntb-catenin signaling, which was accompanied by a decrease of miR-18a, an important modulator of cell cycle proteins [111,112].…”

Section: Breast Cancermentioning

confidence: 99%

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Xuan

Zhang

et al. 2019

FEBS Letters

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) are a major subset of highly conserved non-coding RNAs (ncRNAs) that consist of at least 200 nucleotides and have limited protein-coding potential. Cumulative data have shown that lncRNAs are deregulated in many types of cancer and may control pathophysiological processes of cancer at various levels, including transcription, post-transcription and translation. Recently, lncRNAs have been demonstrated to interact with microRNAs (miRNAs), another major subset of ncRNAs, which regulate physiological and pathological processes by inhibiting target mRNA translation or promoting mRNA degradation. The lncRNA urothelial carcinomaassociated 1 (UCA1) has recently gained much attention as it is overexpressed in many types of cancer and is involved in carcinogenesis. Here, we review the crosstalk between UCA1 and miRNAs during the pathogenesis of cancer, with a focus on cancer-cell proliferation, invasion, drug resistance, and metabolism.

show abstract

Long non-coding RNA UCA1 enhances tamoxifen resistance in breast cancer cells through a miR-18a-HIF1α feedback regulatory loop

Cited by 101 publications

References 37 publications

A three-long noncoding RNA signature as a diagnostic biomarker for differentiating between triple-negative and non-triple-negative breast cancers

A three-long noncoding RNA signature as a diagnostic biomarker for differentiating between triple-negative and non-triple-negative breast cancers

Long Non-Coding RNAs: Key Regulators of Epithelial-Mesenchymal Transition, Tumour Drug Resistance and Cancer Stem Cells

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Contact Info

Product

Resources

About