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Melone, V.;  Salvati, A.;  Brusco, N.;  Alexandrova, E.;  D’agostino, Y.;  Palumbo, D.;  Palo, L.;  Terenzi, I.;  Nassa, G.;  Rizzo, F.; et al. LncRNA Mechanisms in Breast Cancer. Encyclopedia. Available online: https://encyclopedia.pub/entry/40778 (accessed on 20 December 2025).
Melone V,  Salvati A,  Brusco N,  Alexandrova E,  D’agostino Y,  Palumbo D, et al. LncRNA Mechanisms in Breast Cancer. Encyclopedia. Available at: https://encyclopedia.pub/entry/40778. Accessed December 20, 2025.
Melone, Viola, Annamaria Salvati, Noemi Brusco, Elena Alexandrova, Ylenia D’agostino, Domenico Palumbo, Luigi Palo, Ilaria Terenzi, Giovanni Nassa, Francesca Rizzo, et al. "LncRNA Mechanisms in Breast Cancer" Encyclopedia, https://encyclopedia.pub/entry/40778 (accessed December 20, 2025).
Melone, V.,  Salvati, A.,  Brusco, N.,  Alexandrova, E.,  D’agostino, Y.,  Palumbo, D.,  Palo, L.,  Terenzi, I.,  Nassa, G.,  Rizzo, F.,  Giurato, G.,  Weisz, A., & Tarallo, R. (2023, February 02). LncRNA Mechanisms in Breast Cancer. In Encyclopedia. https://encyclopedia.pub/entry/40778
Melone, Viola, et al. "LncRNA Mechanisms in Breast Cancer." Encyclopedia. Web. 02 February, 2023.
LncRNA Mechanisms in Breast Cancer
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This entry is adapted from the peer-reviewed paper 10.3390/ijms24021145

Genomic studies have revealed the multiplicity of processes, including neoplastic transformation and tumor progression, in which lncRNAs are involved by regulating gene expression at epigenetic, transcriptional, and post-transcriptional levels by mechanism(s) that still need to be clarified. In breast cancer, several lncRNAs were identified and demonstrated to have either oncogenic or tumor-suppressive roles. The functional understanding of the mechanisms of lncRNA action in this disease could represent a potential for translational applications, as these molecules may serve as novel biomarkers of clinical use and potential therapeutic targets.

lncRNAs estrogen receptor alpha estrogen signaling

1. Estrogen-Inducible lncRNAs

The application of NGS methods, particularly GRO and RNA-Seq, allowed the identification of a huge number of lncRNAs, many of them appearing to be regulated by estrogenic signaling or having specific roles in estrogen-dependent transcriptional regulation.

1.1. lncRNA H19

The maternally imprinted oncofetal lncRNA H19, physiologically expressed during embryogenesis and down-regulated at birth, was demonstrated to be re-expressed in a variety of cancers and act through different mechanisms [1]. Aberrant expression levels of H19 were identified in different cancer types, including BC, where it acts as an oncogenic factor [2]. A relationship between H19 expression and hormone receptors (both PR and ER) was previously proposed [3]. H19 appeared to be over-expressed in Erα+ MCF7 cells compared to the Erα- MDA-MB-231 cell line [4]. Sun et al. demonstrated that stimulation with 17β-estradiol produced a dose and time-dependent induction of H19 expression in MCF-7 cells. This effect was supposed to be Erα-mediated since Erα inhibition, either through the treatment with ICI 182,780, the specific Erα antagonist, or knock-down, determined its reduction [4]. On the other hand, H19 knock-down decreased BC cell survival and blocked estrogen-induced cell growth, while its over-expression induced cell proliferation [4].
Another study demonstrated the involvement of H19 in the symmetric division of breast cancer stem-like cells (BrCSCs), which resulted in increasing levels of self-renewing [5]. BrCSCs are highly implicated in tumor generation, resistance, and recurrence and, in the cited study, it was demonstrated that H19 inhibited Let-7c expression by acting as a ceRNA (competing endogenous RNA), thus affecting the estrogen-activated Wnt pathway and determining the BrCSC symmetric division [5].

1.2. HOX Transcript Antisense RNA (HOTAIR)

Similar to H19, the expression of the lncRNA HOX transcript antisense RNA (HOTAIR) was regulated in an estrogen-dependent manner [6]. HOTAIR belongs to the mammalian HOX locus, and its structure is devoid of any stem-loops, suggesting this is a pre-miRNA [7]. This lncRNA could be considered a potential diagnostic and clinically actionable marker for different cancer types [7], including BC since its expression profile appears to be up-regulated in both primary tumors and distant metastases compared to adjacent normal tissue [8]. HOTAIR is transcribed from the antisense strand of the HOXC gene locus in chromosome 12, and its promoter contains multiple functional estrogen-response elements (EREs) [6].
From a functional point of view, HOTAIR is involved in epigenetic regulation and plays an important role in several cellular pathways by interacting with polycomb repressive complex 2 (PRC2) [7], which modulates epigenetic silencing in several processes, including neoplastic transformation [9]. PRC2 is a histone methyl transferase complex mainly composed of three major subunits: EZH2, the key factor for methyl transferase activity, SUZ12 and EED, which increase EZH2 RNA binding affinity [7]. HOTAIR localizes and targets PRC2 genome-wide [10] and functions as a molecular scaffold, also interacting with the LSD1 (lysine-specific demethylase 1) complex to regulate gene expression by affecting histone H3 demethylation at lysine 4 [7]. HOTAIR binds PRC2 to the 5’ domain and LSD1 to the 3’ domain affecting, through these two complexes, chromatin remodeling and the expression of different genes involved in a variety of cell functions [10][11].
Concerning estrogenic signaling, Bhan et al. identified the mechanism by which Erα recruits multiple ER-coregulators, such as histone methylases MLL1 and MLL3 and CBP/p300, and binds the HOTAIR promoter region in an E2-dependent manner [6]. Particularly, the HOTAIR promoter is targeted by histone H3K4-trimethylation, histone acetylation, and RNA polymerase II in the presence of E2; on the contrary, the knock-down of both Erα and MLLs down-regulates E2-induced HOTAIR expression [6].

1.3. lncRNA ERINA

The intergenic lncRNA ERINA (estrogen-inducible lncRNA) was identified to be highly expressed in multiple cancer types, especially in Erα+ BC [12]. ERINA was described as an estrogen-responsive oncogenic factor because its knock-down inhibits cell-cycle progression and cancer cell proliferation both in vitro and in xenograft in vivo models, while its over-expression promotes cell growth and cell-cycle progression [13].
This functions as an ERα-responsive gene: an ER-binding element was identified within the ERINA intronic site, and the enrichment of H3K27Ac suggested that this region functions as an enhancer to mediate the estrogen-responsive induction of ERINA [13].
Its oncogenic roles were found to be directly related to an interaction with E2F transcription factor 1 (E2F1). ERINA over-expression induces the sequestration of tumor suppressor retinoblastoma protein 1 (RB1), which normally binds to E2F1, and the release of E2F1, causing the over-expression of its target genes particularly involved in cell-cycle progression [13]. These findings also suggested that ERINA over-expression may contribute to drug resistance and the poor survival of patients with ERα+ BC not responding to endocrine therapies [13].

1.4. Myocardial Infarction-Associated Transcript (MIAT)

Another lncRNA regulated via estrogenic signaling is the myocardial infarction-associated transcript (MIAT) [14].
Significant evidence points to the involvement of MIAT in various diseases and cellular processes [15][16][17][18], and the abnormal expression of this lncRNA was observed in multiple malignancies and in BC [19][20].
Concerning BC, its over-expression was more likely observed in ERα+ BC tissues than in ERα- ones [14]. Li et al. demonstrated that estrogen signaling activation using diethylstilbestrol (DES) allows the dose and time-dependent up-regulation of MIAT in MCF-7 cells. ERα inhibition through either silencing or pharmacological blockade with the specific antagonist ICI 182,780 proved that this occurred through an ERα-dependent mechanism. Moreover, MIAT knock-down allowed decreased DES-induced MCF-7 cell proliferation, while its over-expression increased MCF-7 cell growth [14]. In another study, it was demonstrated that MIAT knock-down allowed the suppression of the epithelial-mesenchymal transition (EMT), decreased the migration and invasion of MCF-7 BC cell lines, and inhibited tumor growth in vivo [21]. MIAT was described as a ceRNA in the modulation of the tumor suppressor dual specificity phosphatase 7 (DUSP7) by uptaking miR-155-5p [21].

1.5. Long Intergenic Non-Protein Coding RNA 472 (LINC00472) and Long Intergenic Non-Protein Coding RNA 1016 (LINC01016)

Among the lncRNAs regulated by ERα, LINC00472 and LINC01016 were also identified [8].
The expression of intergenic LINC00472 correlates with BC progression and patient survival; particularly, its over-expression was found to be associated with low tumor grade, early-stage disease, estrogen or progesterone receptor positivity, and less cancer aggressiveness [22], while lower expression was associated with aggressive tumor features and unfavorable disease outcomes [22][23].
In addition, it was demonstrated to be estrogen-responsive, and an ERα-binding site within its promoter region was predicted and confirmed [23]. Indeed, LINC00472 is up-regulated by ERα, and its inhibition correlates to poor tumor growth and improved patient outcomes [8].
The second intergenic lncRNA, LINC01016, was identified to be highly expressed in BC and a direct ERα transcriptional target [24] since the receptor binds within its promoter region [25]. Its expression correlates with ERα expression in clinical samples and shows prognostic significance in relation to patients’ survival; its over-expression was observed more specifically in ERα+ tumors with more favorable clinical outcomes [26].

1.6. lncRNA DSCAM-AS1 Regulation by Unliganded ERα

Among ERα activities, it is important to define its constitutive regulatory role in the absence of ligand stimulation. This receptor plays a hormone-independent function in the maintenance of BC cell’s epithelial phenotype. Miano et al. reported the lncRNA DSCAM-AS1 among the genes specifically regulated by unliganded ERα (Apo-ERα) in MCF-7 cells [25]. DSCAM-AS1 is a cancer-related lncRNA over-expressed in luminal A, B, and HER2-positive BCs [27]. This lncRNA is implicated in multiple tumorigenic processes, including DNA replication and chromosome segregation [8]. In another study, further evidence of DSCAM-AS1 expression regulated by ERα was demonstrated [28]. In particular, the authors demonstrated the interaction between ERα and the DSCAM-AS1 promoter and how the association between DSCAM-AS1 and hnRNPL led to a more aggressive cancer phenotype [28]. In addition, the knock-down of DSCAM-AS1 reduced the growth of ERα+ BC cells, diminished EMT markers, and limited cell colony formation [8][25].

2. lncRNAs Able to Regulate ERα Expression

lncRNAs are involved in different steps of gene expression, including transcription, mRNA stability, translation, and epigenetic modifications [29]. Among the lncRNAs that stabilize ERα mRNA, TMPO antisense RNA1 (TMPO-AS1) was identified by Mitobe et al. [30]. Its functions are widely recognized in various diseases, especially in human cancers, and previous studies demonstrated that this acts as an oncogenic factor in colorectal cancer, osteosarcoma, cervical cancer, and non-small cell lung cancer [31].
TMPO-AS1 stabilizes ERα transcripts and positively regulates the expression of the receptor through direct binding to ESR1 mRNA [30]. In this way, TMPO-AS1 promotes cell growth and proliferation of ERα+ BC cells both in vivo and in vitro [30].
Another mechanism involved in ERα stability maintenance was defined for lncRNA MIR2052HG [32], which foresees that this lncRNA regulates lemur tyrosine kinase 3 LMTK3, which is responsible for ERα stability through the PKC/MEK/ERK/RSK1 axis via EGR1 (early growth response protein 1) [32]. Functionally, MIR2052HG interacts with EGR1 and facilitates its recruitment to the LMTK3 gene promoter. On its end, LMTK3 maintains ERα levels both by reducing protein kinase C (PKC) activity, determining an increment of ESR1 transcription through AKT/FOXO3, and by reducing ERα degradation mediated by the PKC/MEK/ERK/RSK1 axis [32]. To confirm this evidence, the depletion of MIR2052HG in BC cells decreased LMTK3 expression and cell growth [32].
In summary, MIR2052HG directly interacts with the EGR1 protein, enhancing LMTK3 transcription and thus sustaining ESR1 expression and stabilizing ERα protein [32]. Furthermore, the inhibition of MIR2052HG in BC cell lines could decrease ERα expression and cell proliferation [33].

3. Enhancer RNAs (eRNAs)

In the beginning, enhancers were defined as DNA fragments located on chromatin, controlling transcription as cis-acting factors. Subsequently, the transcripts derived from active enhancers were identified, and these were named enhancer RNAs (eRNAs) [34][35][36][37]. Enhancer RNAs (eRNAs) may be lncRNAs transcribed bi-directionally by polymerase II from the DNA sequences of enhancer regions marked by H3K27ac and H3K4me1 [38]. Their function is not well defined, but it is known that these lncRNAs are able to increase the expression of target genes and stabilize the binding of active transcription factors when stimulated [38]. On the one hand, eRNAs link DNA enhancers generating them, to target gene promoters, thus aiding functional chromosome architecture formation [39]. On the other hand, they act during the release of paused RNA polymerase II in order to induce transcriptional activation [40][41].
In estrogenic signaling, active ERα is predominantly located at the enhancer regions [42][43]. Genome-wide studies showed that this receptor, after the activation by 17β-estradiol, could induce a global increase in the transcription of eRNAs close to the enhancers of estrogen-regulated coding genes [39]. Notably, it confirmed the existence of two categories of enhancers, both of which showed strong ERα binding and generated RNAs that could be activated or repressed following estrogen exposition [44]. Using the genome-wide nascent transcript profiles in BC cells, Yang et al. identified a group of eRNAs essential for estrogen-induced transcriptional repression [44]. In particular, they described the mechanisms by which the eRNAs TM4SF1 and EFEMP1 not only stabilize promoter-enhancer interactions but also recruit ERα to the enhancer regions to facilitate the formation of a functional transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from the designated enhancers and suppresses the transcription of target genes [44]. ERα directly binds eRNAs through its DNA-binding domain [44].
In another study using ChIP-Seq, a global profile of ERα co-activator thymine DNA glycosylase (TDG), which plays an essential role in DNA demethylation, was generated in response to 17β-estradiol in the MCF7 BC cell line [45]. Following estrogen stimulation, TDG was co-recruited with ERα, RNA Pol II, and other co-regulators to enhancer regions marked by histone modifications indicative of active enhancers [45]. Contrarily, TDG depletion inhibited the estrogen-mediated transcription of eRNAs and the transcription of ERα-target genes [45].
Table 1. Cellular functions of lncRNAs in BC.
LncRNAs Expression in BC Regulation Cellular Functions References
lncRNA H19 Up-regulation Estrogen-dependent Proliferation, tumorigenesis, migration, invasion, and EMT [2][4][5]
HOTAIR (HOX transcript antisense RNA Up-regulation Estrogen-dependent Proliferation, invasion, migration, survival, epigenetic regulation, and chemotherapy resistance [6][9]
LncRNA ERINA Up-regulation Estrogen-dependent Proliferation, survival, and chemotherapy resistance [13]
MIAT
(myocardial infarction-associated transcript)		 Up-regulation Estrogen-dependent Proliferation, migration, invasion, chemotherapy resistance, and EMT [14]
LINC00472 Up-regulation Estrogen-dependent Proliferation, survival, migration, and invasion [22][23]
LINC01016 Up-regulation Estrogen-dependent Proliferation and survival [26]
LncRNA DSCAM-AS1 Up-regulation Estrogen-independent Tumorigenic processes, DNA replication, chromosome, segregation, survival, and EMT [25][28]
TMPO-AS1 (TMPO antisense RNA1) Up-regulation Regulation of ERα expression Proliferation and cell growth [30]
MIR2052HG Up-regulation Regulation of ERα expression Proliferation and cell growth [32][33]

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Noemi Brusco
, Elena Alexandrova , Ylenia D’Agostino , Domenico Palumbo ,
Luigi Palo
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Ilaria Terenzi
, Giovanni Nassa , Francesca Rizzo , Giorgio Giurato , Alessandro Weisz , Roberta Tarallo
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    ${ selectedItem.replyTextCharacter }/${ selectedItem.replyMaxCharacter }
    Submit
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