Long Noncoding RNAs in Breast Cancer: Comparison
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Please note this is a comparison between Version 2 by Dean Liu and Version 1 by mengwen Zhang.

Breast cancer is a common cancer in women and a leading cause of mortality. With the early diagnosis and development of therapeutic drugs, the prognosis of breast cancer has markedly improved. Chemotherapy is one of the predominant strategies for the treatment of breast cancer. Taxanes, including paclitaxel and docetaxel, are widely used in the treatment of breast cancer and remarkably decrease the risk of death and recurrence. Taxane resistance caused by multiple factors significantly impacts the effect of the drug and leads to poor prognosis. Long noncoding RNAs (lncRNAs) have been shown to play a significant role in critical cellular processes, and a number of studies have illustrated that lncRNAs play vital roles in taxane resistance.

  • breast cancer
  • long noncoding RNAs
  • taxane resistance

1. Introduction

Breast cancer is the most frequently diagnosed cancer in women and the leading cause of death worldwide. According to GLOBOCAN 2020, breast cancer was the most commonly diagnosed cancer, with an estimated 2.3 million newly diagnosed cases [1]. With early diagnosis and development of therapeutic drugs, the prognosis of breast cancer has markedly improved. Chemotherapy, endocrine therapy, HER2 (human epidermal growth factor receptor 2)-targeted therapy, and immunotherapy have been applied for diverse breast cancers. However, drug resistance remains an important factor in the poor prognosis of patients with breast cancer.
As an important treatment strategy for breast cancer, chemotherapy is widely used in the treatment of breast cancer and remarkably decreases the risk of death and recurrence. Taxanes, including paclitaxel and docetaxel, are basic chemotherapeutic agents used to treat patients with breast cancer. Although taxanes suppress tumor growth and improve survival in advanced breast cancer, the development of resistance is inevitable and results in treatment failure. However, the mechanisms of taxane resistance are not fully understood, and further investigation into taxane resistance mechanisms is necessary to identify potential biomarkers and develop novel treatments aimed at overcoming taxane resistance.
Noncoding RNAs (ncRNAs) are a class of transcripts that are encoded by the genome but are mostly not translated into proteins. NcRNAs have been found to be dysregulated in various cancers and linked to cancer development [2,3,4,5][2][3][4][5]. LncRNAs are important members of the ncRNA family that are longer than 200 nucleotides and have been shown to play a significant role in critical cellular processes, such as transcription, translation, epigenetic control, stem cell differentiation, autophagy, and apoptosis. As lncRNAs have been implicated in chemotherapy resistance [6,7[6][7][8][9],8,9], exploring their role in taxane resistance has become a hot research topic in recent years.

2. Mechanisms of Taxane Resistance in Breast Cancer

The taxane class is a series of derivatives synthesized by isolating the active antitumor component from plants and structurally modifying the active component obtained. Taxanes mainly include paclitaxel, docetaxel, and derivatives with a paclitaxel backbone structure. Paclitaxel is a taxane diterpene isolated from the bark of Taxus brevifolia [10,11,12][10][11][12]. Docetaxel is a semisynthetic product of precursors extracted from Taxus baccata L. that is structurally similar to paclitaxel [13]. Taxanes have been used to treat certain types of cancers. In particular, the use of taxanes in breast cancer is an important breakthrough that has greatly improved the prognosis of patients with breast cancer [14,15][14][15]. By binding to a hydrophobic cleft in β-tubulin [16], paclitaxel and docetaxel affect the dynamic balance between α- and β-tubulin dimers and microtubules, promoting the assembly of tubulin into microtubules and facilitating microtubule polymerization, blocking their depolymerization into subunits, causing cells to arrest in the G2 and M phases, and leading to abnormal mitosis or cessation of cell division, ultimately causing cell death [17,18,19][17][18][19]. Taxane-induced microtubule stabilization causes Bcl-2 phosphorylation, triggering a cascade of events leading to apoptosis [20]. Chemotherapy resistance is a major cause of cancer treatment failure, resulting in death in over 90% of patients with metastatic cancer [21]. As one of the standard strategies for breast cancer treatment, taxane resistance remains a major obstacle affecting prognosis. Therefore, understanding the mechanism of taxane resistance will help to identify biomarkers and develop new therapeutic approaches to overcome taxane resistance in breast cancer. The major mechanisms that mediate taxane resistance include (1) alteration of tubulin isotypes and mutations; (2) changes in microtubule-associated proteins (MAPs); (3) drug transport and efflux; (4) deregulation of cell death; (5) alterations in proliferation signaling pathways and the epithelial-to-mesenchymal transition (EMT) (Figure 1).
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Figure 1. Molecular mechanisms of taxane resistance in breast cancer. The diagram illustrates some of the major mechanisms that are known to contribute to taxane resistance in breast cancer. Upregulated tubulin isotypes and mutations, changes in MAPs, and drug export transporters have been associated with reduced taxane efficacy. Furthermore, upregulated antiapoptotic proteins, upregulated proliferation signaling pathways, and EMT have been linked with increased proliferation after taxane treatment.

3. Long Noncoding RNAs

The transcription process involves production of both protein-coding messenger RNAs (mRNAs) and noncoding RNAs (ncRNAs) [107][22]. As a subclass of noncoding RNAs, lncRNAs consist of more than 200 nucleotides. Most lncRNAs have the same characteristics as mRNAs but are usually transcribed from fewer exons than coding RNAs and lack an open reading frame [108,109][23][24]. In general, lncRNAs are localized to the nucleus but can also be detected in the cytoplasm [110][25]. They are transcribed by RNA polymerase II, undergo 5′ capping, 3′ cleavage, and polyadenylation and produce mature lncRNAs through splicing, although the process is less efficient than that of mRNA splicing [108,111][23][26]. LncRNAs are typically classified into five categories based on their location relative to adjacent protein-coding genes, including intergenic lncRNAs (lincRNAs), antisense lncRNAs, sense lncRNAs, intronic lncRNAs, and bidirectional lncRNAs [112,113][27][28]. LncRNA expression is mainly tissue specific, suggesting that lncRNAs may play a functional role in physiological and biological processes [114][29]. Although the roles of most lncRNAs have not been verified, it has been shown that lncRNAs are involved in many areas of genome function, including epigenetics, gene transcription, splicing, and translation, as well as fundamental biological processes, such as cell cycle progression and differentiation [115][30]. In addition, lncRNAs perform cytoplasmic functions, mainly acting as miRNA sponges, regulating translation of specific mRNAs, and interacting with various signaling proteins [5]. Overall, lncRNAs are a group of diverse regulatory ncRNAs with different properties, locations, and mechanisms of action. The function of lncRNAs depends on their subcellular localization [113,116][28][31]. Several mechanisms of action have been proposed for lncRNAs (Figure 2).
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Figure 2. Mechanisms of action of lncRNAs. (A) Act as signals: Signaling lncRNAs respond to stimuli, receive signals, and interact with chromatin modification enzymes to prevent transcription. (B) Act as decoys: (a) Decoy lncRNAs have high affinity for selective transcription factors, and after binding to lncRNAs, the transcription process is inhibited because transcriptional regulators do not bind to DNA. (b) LncRNAs can also act as “sponges” for miRNAs, blocking the inhibitory effect of miRNAs on their downstream target mRNAs and thus regulating gene expression. (C) Act as guides: guide lncRNAs assemble transcription factors at specific loci and influence regulation of chromatin modification, thereby regulating transcription. (D) Act as scaffolds: Scaffold lncRNAs assemble RNA—protein complexes and promote or suppress transcription by suppressing or activating target genes.
The first mode of action involves signaling. LncRNAs are specifically transcribed under different stimuli and act as signaling molecules to participate in specific pathways, regulating the transcription of downstream genes. For example, lncRNA Kcnq1ot1 and Air mediate transcriptional silencing of multiple genes by interacting with chromatin and recruiting the chromatin-modifying machinery [117][32]. XIST, which mediates X chromosome inactivation in females, is also associated with this mechanism. During female development, Xist RNA is expressed from the inactive X chromosome and acts as a ‘coat’ on the chromosome it is transcribed from, leading to chromosome-wide repression of gene expression [118][33]. LncRNAs can also act as decoys and bind directly to selective transcription regulatory factors or RNA. As a result of lncRNA binding, transcription is repressed owing to lack of binding of transcription regulatory factors to DNA. For example, lncRNA PANDA can bind to NF-YA, a transcription factor responsible for the activation of apoptosis-related genes, resulting in suppression of its target genes [119][34]. Many lncRNAs also act as “sponges” for miRNA and block inhibition of miRNA on its downstream target mRNA, thereby indirectly regulating gene expression; examples are TUG1 and MEG3, which can isolate miRNA from mRNA and protein targets, altering protein translation [120][35]. Several studies have also revealed the lncRNA—mRNA interaction; lncRNAs that possess Alu elements can bind to the 3′UTR of mRNA and mediate mRNA degradation [121,122][36][37]. The third mode is guide-mediated action, in which lncRNAs guide chromatin modifiers or transcription factors to target genes and help them to localize appropriately at transcriptional loci, regulating transcription. It has been found that this transcriptional regulation by lncRNA mediators can occur through a cis- or trans-acting mechanism. An example of a cis-acting lncRNA is HOTTIP (HOXA Distal Transcript Antisense RNA), which promotes expression of the gene HOXA, and lncRNAs such as HOTAIR are able to alter and regulate epigenetic states in cells through targeting of the chromatin-modifying complex in trans [117][32]. In scaffold action, scaffold lncRNAs play an important structural role in assembling RNA—protein complexes, thereby promoting or suppressing transcription by activating or repressing target genes. For example, TINCR scaffolds the RNA-binding protein staufen1 with epidermal differentiation-promoting mRNAs that bind the TINCR box motif and promote its posttranscriptional stabilization. HOTAIR (HOX Transcript Antisense Intergenic RNA) scaffolds PRC2 proteins, thereby affecting chromatin accessibility and nuclear architecture and repressing transcription [123][38]. In general, lncRNAs regulate gene expression at three levels: epigenetic, transcriptional, and posttranscriptional regulation. Epigenetic regulation is pretranscriptional regulation of eukaryotic gene expression, which mainly includes chromosomal architecture, histone modification, and DNA methylation and is an important part of gene expression regulation. LncRNAs usually combine with DNA, histone-modifying enzymes and transcription factors to participate in the pretranscriptional regulation of genes. As mentioned above, HOTAIR interacts with PRC2 to silence genes via scaffold action. Other lncRNAs, such as ANRIL, H19, and XIST, also repress gene transcription by recruiting protein complexes, such as histone modifiers and chromatin remodeling complexes [124][39]. Transcriptional regulation is the most important form of regulation of gene expression. LncRNAs can participate in the transcriptional regulation of target genes by regulating transcription of neighboring protein-coding genes, interacting with transcription factors, and forming triple helix complexes with DNA. LncRNAs can directly regulate gene expression by influencing the activity of enhancers [114][29]; lncRNAs themselves can also act as enhancer RNAs (eRNAs) to influence chromatin interactions [125][40]. In addition, lncRNAs can bind with proteins and mRNAs to form ribonucleoprotein complexes, which regulate posttranscriptional gene regulation. LncRNAs can also act as molecular decoys for miRNAs, sequestering miRNAs, and therefore inhibiting their regulatory effects on gene expression [126][41]. For example, lncRNA H19 has been shown to sponge and inhibit miR-675, suggesting a competing endogenous RNA (ceRNA) role for H19 lncRNA [127][42]. Furthermore, lncRNAs are involved in the translation machinery and regulate mRNA translation [113][28].

4. LncRNAs and Taxane Resistance

LncRNAs are recognized as important regulators of gene expression in cancer. Many lncRNAs have been implicated in cancer initiation and progression [108,128][23][43]. Abnormal expression of lncRNAs is closely related to tumor occurrence, metastasis, and tumor stage [129,130][44][45]. Furthermore, lncRNAs can directly or indirectly regulate a variety of pathways related to chemotherapy resistance, such as changes in drug efflux, inhibition of apoptosis pathways, and promotion of EMT [131,132,133][46][47][48]. As mentioned above, taxane resistance is a growing challenge in modern breast cancer chemotherapy, but the role of lncRNAs in mediating taxane resistance and susceptibility is not yet fully understood. However, several mechanisms are believed to be associated with taxane resistance induced by lncRNAs. First, ABC overexpression leads to enhanced drug efflux. ABC proteins, such as P-gp, ABCG2, and MRP, are frequently overexpressed in many types of cancers [134][49]. Multidrug resistance can be induced by overexpression of ABC efflux transporters due to specific lncRNAs [135][50]. A number of studies have shown that lncRNAs play a key role in increasing the outflow of a wide range of chemotherapeutic agents from a variety of cancer cells [136,137,138][51][52][53]. For example, UCA1 confers paclitaxel resistance through miR-129/ABCB1 axis in ovarian cancer [139][54]. In colorectal cancer, LINC00473 promotes paclitaxel resistance by activating the Bcl-2-related pathway and increases the LRP and MDR1 expression of MDR genes [140][55]. Second, many chemotherapeutic agents inhibit the proliferation of cancer cells by promoting apoptosis: lncRNAs associated to apoptotic pathways have been linked to multidrug resistance [132][47]. LncRNAs can protect cancer cells by inhibiting apoptosis. A previous study reported that after silencing LINC00511 expression, Bax and cleaved-caspase-3 increased with more cervical cancer cells arrested at the G1 phase [141][56]. In docetaxel-resistant lung adenocarcinoma cells, lncRNA CCAT1 was upregulated, and further study revealed that CCAT1 promotes chemoresistance by targeting the let-7c/Bcl-xl pathway [142][57]. Third, lncRNAs play a role in the EMT through signaling pathways, such as Wnt/β-Catenin and AKT/mTOR. Resistance/sensitivity to many chemotherapeutic agents has been associated with EMT-related lncRNAs [132][47]. In gastric cancer, lncRNA ZFAS1 can induce EMT via the Wnt/β-catenin pathway, thereby promoting chemotherapeutic tolerance [143][58]. Similarly, lncRNAs may mediate taxane resistance through these mechanisms in breast cancer (Figure 3). 
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Figure 3. LncRNA-mediated mechanisms of taxane resistance in breast cancer. LncRNAs mediate taxane resistance by multiple molecular mechanisms, such as enhanced drug efflux, inhibition of apoptosis, promotion of proliferation signaling pathways and EMT, and alteration of MAPs.

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