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Agirre, X. LncRNAs for Multiple Myeloma. Encyclopedia. Available online: https://encyclopedia.pub/entry/9692 (accessed on 13 December 2025).
Agirre X. LncRNAs for Multiple Myeloma. Encyclopedia. Available at: https://encyclopedia.pub/entry/9692. Accessed December 13, 2025.
Agirre, Xabier. "LncRNAs for Multiple Myeloma" Encyclopedia, https://encyclopedia.pub/entry/9692 (accessed December 13, 2025).
Agirre, X. (2021, May 17). LncRNAs for Multiple Myeloma. In Encyclopedia. https://encyclopedia.pub/entry/9692
Agirre, Xabier. "LncRNAs for Multiple Myeloma." Encyclopedia. Web. 17 May, 2021.
LncRNAs for Multiple Myeloma
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This entry is adapted from the peer-reviewed paper 10.3390/cancers13081976

MM is a hematological neoplasm that is still considered an incurable disease. Besides established genetic alterations, recent studies have shown that MM pathogenesis is also characterized by epigenetic aberrations, such as the gain of de novo active chromatin marks in promoter and enhancer regions and extensive DNA hypomethylation of intergenic regions, highlighting the relevance of these non-coding genomic regions. A recent study described how long non-coding RNAs (lncRNAs) correspond to 82% of the MM transcriptome and an increasing number of studies have demonstrated the importance of deregulation of lncRNAs in MM. 

lncRNAs multiple myeloma RNA-based therapy

1. Introduction

Multiple myeloma (MM) is a hematological neoplasm characterized by the uncontrolled aberrant clonal proliferation of plasma cells (PCs) in the bone marrow [1]. This disease is the second most common hematological malignancy, after non-Hodgkin lymphoma [2][3], affecting elderly patients with a median age of 65 years [4]. Despite the latest advances in treatment strategies, which have significantly increased patient survival, MM is still considered an incurable disease, with a median overall survival of 7 years.

MM is a very heterogeneous disease, which is reflected in the inter-individual differential diagnosis and survival of patients. Different studies have associated this variability with a wide range of genetic and epigenetic alterations present in MM patients [5][6], including distinct molecularly defined subtypes with different features [7]. Regarding the genetic variability, MM is divided into hyperdiploid (HRD) and non-HRD subtypes [7]. HRD MM is characterized by the trisomy of chromosomes 3, 5, 7, 9, 11, 15, 19 and 21 [6], whereas non-HRD MM is characterized by translocations of the immunoglobulin (Ig) alleles. The majority of these translocations affect chromosome 14, where the Ig H-chain is located [6][7]. However, Ig translocations can also affect the kappa and lambda light chains, the co-occurrence of which is common with HRD MM. Besides, some of these light-chain translocations are associated with a poor outcome for MM patients, as is the case for IgL-MYC translocations [8]. Some of the common heavy-chain translocations are also considered as high-risk prognostic factors, such as t(4;14) and t(14;16), which affect MMSET and MAF genes, respectively [6][7][9]. Epigenetic aberrations of the DNA methylation and histone modifications are also thought to play an important role in MM pathogenesis. The study of global DNA methylation of MM has led to the identification of a highly heterogeneous DNA methylation pattern, which results in extensive DNA hypomethylation of intergenic regions and DNA hypermethylation associated with intronic and enhancer regions [2][5]. In addition, the study of histone modifications in MM has revealed a de novo gain of active chromatin marks preferentially located in regulatory elements, such as enhancer and promoter regions, which arise from heterochromatic regions in normal B cells [10][11][12]. These results suggest the possibility that these epigenetically regulated non-coding genomic regions could lead to the transcription of non-coding RNA genes (ncRNAs) and, in particular, to the expression of long non-coding RNAs (lncRNAs), which may play a relevant role in the pathobiology and clinical outcome of MM [13]. Nowadays, studies about the role of certain lncRNAs in MM are emerging. However, more comprehensive analyses are required to better understand their function in this disease. In this review, we summarize the current knowledge regarding the role of lncRNAs in the development and outcome of MM and discuss the possibility of lncRNAs as targets for the development of novel RNA-based therapeutic strategies for MM patients.

2. Features of lncRNAs

Traditionally, cellular functions of DNA and proteins have overshadowed the roles of RNAs. In recent years, the development of high-throughput techniques, such as RNA sequencing (RNA-seq), has brought great advances in the understanding of the cell transcriptome. So far, it is known that, although only 1–2% of the human genome is translated into proteins, around 70–90% of it is transcribed into RNA, resulting in a huge amount of ncRNAs [14]. Among these ncRNA genes, lncRNAs are defined as those non-coding transcripts longer than 200 nt that do not encode proteins, with open reading frames (ORFs) smaller than 100 amino acids, and with a lack of or low coding potential. However, the latest RNA-seq studies have shown that some lncRNAs contain cryptic ORFs, which could encode for small ORFs or non-conserved peptides [15][16][17].

The characteristics of lncRNAs may differ from each other and they can be capped at the 5′end, spliced and/or polyadenylated (poly(A)+). Remarkably, transcripts with the poly(A)+ tail have higher stability than those with poor or no polyadenylation. On the other hand, there are lncRNAs that can present both polyadenylated and non-polyadenylated isoforms, such as MALAT1 (metastasis associated lung adenocarcinoma transcript 1) or NEAT1 (nuclear paraspeckle assembly transcript 1) [18][19]. Although the size of lncRNAs varies between 200 nt and more than 1 MB (known as macro lncRNAs), 42% of lncRNAs only present two exons [19][20]. In contrast to mRNAs, which are located at the cytosol, lncRNAs can be located either in the nucleus or in the cytoplasm, where they can exert various functions. Thus, regarding the location where lncRNAs act and their transcription site, they are capable of acting as cis and/or trans transcripts [15][21]. Cis lncRNAs are known to influence the expression and/or chromatin states of their neighboring genes, while trans lncRNAs act over distal genes [22][23][24]. Interestingly, lncRNAs are cell- and tissue-specific, and they may affect different biological processes, such as chromosome conformation, imprinting of genomic loci, or gene and protein regulation [15][25]. lncRNAs have the ability to regulate at DNA, RNA and protein levels, and their functions can be divided into four different groups depending on their molecular mechanisms [18][26]: (1) signal lncRNAs are regulatory molecules that can trigger the transcription of other genes by their presence. They can infer chromatin states, affect gene imprinting or mark certain spaces, times or stages for gene regulation, such as Air or PANDA (p21-associated ncRNA DNA damage activated) [26][27]. (2) Decoy lncRNAs are transcripts that bind to targets and prevent them from binding to their own targets, thus leading to the alteration of post-transcriptional control. This type of lncRNA can act as an miRNA sponge, binding to miRNAs thanks to their complementary sequence (Figure 1) [26]; PTENP1 (phosphatase and tensin homolog pseudogene 1), for example, leads to tumor suppressor activity due to the decoy of different miRNAs [28][29][30]. (3) Guide lncRNAs can regulate gene expression through the recruitment and re-localization of ribonucleoprotein complexes at specific chromatin loci, such as MEG3 (maternally expressed 3), which guides the EZH2 subunit to TGFβ-regulated genes (Table 1) [18][31][32]. (4) Scaffold lncRNAs can act as central platforms upon the assembly of different ribonucleoprotein complexes, affecting their molecular components (Figure 1) [32]; for instance, HOTAIR (HOX transcript antisense intergenic RNA) adopts a four-module secondary structure for the interaction with polycomb repressive complex 2 (PRC2) (Table 1), promoting gene repression [18][26].

Cancers 13 01976 g001 550

Figure 1. Mechanisms by which MALAT1 acts in MM cells. (A) MALAT1 acts as scaffold lncRNA, binding to PARP1 protein, which binds to a complex of DNA-repair enzymes consisting of LIG3 among others. Then, the protein–MALAT1 complex repairs the damaged DNA, triggering the proliferation of MM cells. However, when binding of MALAT1 and PARP1 does not occur, damaged DNA is not repaired, triggering MM cell death [33]. (B) MALAT1 can also act as a miRNA sponge (decoy), binding to different miRNAs such as miR-1271-5p, a tumor-suppressor miRNA that negatively regulates SOX13. Binding of MALAT1 and miR-1271-5p triggers overexpression of SOX13 and proliferation of MM cells, whereas knockdown of MALAT1 releases miR-1271-5p, which binds and prevents translation of SOX13. MM = multiple myeloma.

Table 1. Summary of deregulated lncRNAs in MM. MM = multiple myeloma; KD = knockdown; UR = upregulation; up = upregulated; down = downregulated; NA = not available; PFS = progression-free survival; OS = overall survival.

Gene Location Gene Type Expression in MM Molecular Mechanism Molecular Interaction in MM Biological Effect after lncRNA KD Biological Effect after lncRNA UR Prognosis in MM References
ANRIL 9p21.3 Antisense Up Decoy Binds to miR-34a, miR-125a, miR-186 and miR-
411–3p		 Decreases cellular proliferation and increases apoptosis NA High expression levels associated with worse PFS and OS [34][35]
BM742401 18q11.2 LincRNA Down NA NA NA Decreases cell migration Methylated lncRNA associated with worse OS [36]
Circ_0000190 1q42.12 Circular lncRNA Down NA NA NA NA High expression levels associated with better PFS and OS [37][38][39]
CRNDE 16q12.2 LincRNA Up Decoy Binds to miR-451 Decreases cellular proliferation, increases apoptosis and triggers cell cycle arrest NA High expression levels associated with worse OS [40][41]
DARS-AS1 2q21.3 Antisense Up under hypoxia Decoy Interacts with RBM39 and HIP-1α, suppressing mTOR pathway Decreases cellular proliferation and increases apoptosis. Decreases tumorigenesis in vivo. Its upregulation reduces the sensitivity to bortezomib in vitro NA NA [42]
ENSG00000249988 4p15.33 LincRNA Up NA NA NA NA High expression levels associated with worse PFS andbetter OS [13]
ENSG00000254343 8q24.12 LincRNA Up NA NA NA NA High expression levels associated with worse PFS [13]
FEZF1-AS1 7q31.32 Antisense Up Decoy Binds to miR-610 and regulates AKT3 Decreases cellular proliferation, increases apoptosis and triggers cell cycle arrest NA NA [43]
GAS5 1q25.1 Processed transcript Down NA NA NA Decreases cellular proliferation NA [44]
H19 11p15.5 Processed transcript Up Decoy Binds to miR-152-3p and miR-29b-3p Decreases cellular proliferation, increases apoptosis and triggers cell cycle arrest NA High expression levels associated with worse PFS [45][46][47]
HOTAIR 12q13.31 Antisense Up NA Activates NF-κB pathway Decreases cellular proliferation, triggers cell cycle arrest and decreases chemoresistance to dexamethasone NA NA [21][48][49][50]
HOXB-AS1 17q21.32 Antisense Up Scaffold Scaffold for ELAVL1. Interacts with FUT4-mediated Wnt/β-catenin pathway Decreases cellular proliferation and increases apoptosis NA NA [51]
IRAIN 15q26.3 Antisense Down Decoy Binds to miR-125b and regulates IGF-1 signaling NA Increases apoptosis NA [52][53]
LINC00152 2p11.2 LincRNA Up Decoy Binds to miR-497 Decreases cellular proliferation, increases apoptosis and triggers cell cycle arrest. Decreases tumorigenesis in vivo NA High expression levels associated with worse OS [54]
LINC00461 5q14.3 LincRNA Up NA NA Decreases cellular proliferation and increases apoptosis NA High expression levels associated with worse OS [55][56][57]
LINC00515 21q21.3 LincRNA Up Decoy Binds to miR-140-5p Increases apoptosis NA NA [58]
LINC00665 19q13.12 LincRNA Up Decoy Binds to miR-214-3p Decreases cellular proliferation and increases apoptosis NA NA [59]
LINC01234 12q24.13 LincRNA Up Decoy Binds to miR-124-3p Decreases cellular proliferation and increases apoptosis. Decreases cell proliferation and tumor growth in vivo NA High expression levels associated with worse OS [60]
lnc-ANGPTL1-3 1q25.2 Antisense Up Decoy Binds to miR-30a-3p Increases the sensitivity to bortezomib NA High expression levels associated with worse OS [61]
lnc-TCF7 5q31.1 NA Up NA NA NA NA High expression levels associated with worse PFS and OS [62]
LUCAT1 5q14.3 LincRNA Up NA Activates the TGF-β signaling pathway Decreases cellular proliferation, increases apoptosis and triggers cell cycle arrest NA High expression levels associated with shorter five-year survival [63]
MALAT1 11q13.1 LincRNA Up Decoy and Scaffold Binds to miR-1271-5p, miR-181a-5p and miR-509-
5p. Scaffold for PARP1		 Decreases cellular proliferation and increases apoptosis NA High expression levels associated with worse PFS and OS [64][65][66][67][68][69][70][33]
MEG3 14q32.2 LincRNA Down Decoy Binds to miR-181a NA Decreases cellular proliferation and increases apoptosis High expression levels associated with better PFS and OS [71][72][73][74]
MIAT 22q12.1 LincRNA Up Decoy Binds to miR-29b Sensitizes MM cells to bortezomib NA High expression levels associated with worse PFS and OS [75][76]
NEAT1 11q13.1 LincRNA Up Decoy Binds to miR-214 and miR-125a Decreases cellular proliferation NA High expression levels associated with worse PFS and OS [77][78][79][80]
OIP5-AS1 15q15.1 Processed transcript Down Decoy Binds to miR-410 and miR-27a-3p NA Decreases cellular proliferation and increases apoptosis NA [81][82]
PCAT-1 8q24.21 LincRNA Up Decoy Binds to miR-129 Increases apoptosis and sensitizes MM cells to bortezomib NA NA [83][84]
PDIA3P 1q21.1 Pseudogene Up NA NA Decreases cellular proliferation. Increases the sensitivity to bortezomib NA High expression levels associated with worse OS [85]
PDLIM1P4 3q12.1 Pseudogene Up NA NA NA NA High expression levels associated with worse PFS and OS [13]
PRAL 17p13.1 NA Down Decoy Binds to miR-210 NA Decreases cellular proliferation and increases apoptosis. Increases the anti-tumor effect of bortezomib High expression levels associated with better PFS and OS [86][87]
PVT1 8q24.21 Processed transcript Up Decoy Binds to miR-203a. It is inhibited by BRD4 Decreases cellular proliferation and increases apoptosis NA NA [88][89]
SMILO 1q42.2 LincRNA Up NA Regulates IFN pathway Decreases cellular proliferation and increases apoptosis NA High expression levels associated with better OS [13]
SNHG16 17q25.1 Processed transcript Up Decoy Binds to miR-342-3p Decreases cellular proliferation, increases apoptosis and triggers cell cycle arrest NA NA [90]
SOX2OT 3q26.3 Sense overlapping Up Decoy Binds to miR-144-3p Decreases cellular proliferation, increases apoptosis and triggers cell cycle arrest. Decreases tumor growth in vivo NA NA [91]
ST3GAL6-AS1 3q12.1 Antisense Up NA NA Decreases cellular proliferation, increases apoptosis and triggers cell cycle arrest NA High expression levels associated with worse PFS [92][93]
TUG1 22q12.2 Antisense Up Decoy Binds to miR-29b-3p and targets HDAC4 Decreases cellular proliferation and increases apoptosis NA NA [44][94]
UCA1 19p13.12 Processed transcript Up Decoy Binds to miR-1271-5p and miR-331-3p Decreases cellular proliferation and increases apoptosis NA High expression levels associated with worse OS [95][96]
XLOC_013703 20p11.21 NA Down NA Involved in NF-κB signaling activation NA Decreases cellular proliferation and increases apoptosis NA [97]

3. Role of lncRNAs in the Pathobiology of MM

Diverse studies have pointed to the importance of lncRNAs in different biological processes, such as immune response, cell differentiation, gene expression modulation and chromatin reorganization [98][99]. Intriguingly, their deregulation also contributes to the development of carcinogenesis, metastasis and even anti-cancer treatment resistance [64]. The deregulation of the expression of lncRNAs can thus impact on relevant pathways involved in the pathogenesis and/or progression of certain human tumors, including MM [44][71]. We have recently demonstrated that 82% of the transcriptome, including coding genes and all types of polyA+ and non-polyA lncRNAs, in plasma cells from MM correspond to lncRNAs, compared to 18% of coding genes [13].

Some deregulated lncRNAs in MM also appear deregulated in the same way in other types of human cancer: for example, HOTAIR is upregulated in hepatocellular carcinoma (HCC), PDIA3P (protein disulfide isomerase family A member 3 pseudogene 1) in lung cancer, and LINC00461 in both HCC and lung cancer, all three of them being also upregulated in MM [48][49][50][55][56][57][100]. PRAL (P53 regulation associated lncRNA) is downregulated in HCC, lung cancer and MM, and GAS5 (growth arrest specific 5) in breast, prostate, renal cancer and MM [44][86][87][101][102]. However, there are lncRNAs that are deregulated in MM while they show the opposite direction of expression in other neoplasms. For instance, MALAT1 is upregulated in MM, lung cancer, gallbladder cancer, colorectal carcinoma and HCC, whilst this lncRNA is downregulated in colorectal and glioma cancer [65][103][104]. NEAT1 is also upregulated in MM, lung cancer and HCC, but is downregulated in acute promyelocytic leukemia [105]. Finally, Circ_0000190 is downregulated in MM and gastric cancer, whereas it displays overexpression in lung cancer [37][38][39]. These results highlight the cell- and tissue- specificity of lncRNAs, showing that their deregulation—and thus, their potential function—needs to be addressed in each tumor. For example, MALAT1 (one of the most widely studied lncRNAs [103]) and NEAT1 are able to bind or interfere with different molecules and pathways depending on the tissue or disease (Table 1) [77][106]. MALAT1 acts as an miRNA sponge binding to miR-1271-5p (Figure 1), miR-181a-5p and miR-509-5p in MM, to miR-195 in HCC or to miR-206 and miR-363-3p in gallbladder cancer [64][66][67][68][69]. In the case of NEAT1, it binds to miR-125a in MM and to miR-193a-3p in lung adenocarcinoma, among others [77][106]. Usually, the expression of lncRNAs and miRNAs is negatively correlated. Therefore, overexpression of one lncRNA could trigger the downregulation of miRNAs, whereas downregulation of one lncRNA could promote the overexpression of different miRNAs [34][77]. Likewise, there are other examples of lncRNAs which act as miRNA sponges in MM (Table 1). In MM, some of these lncRNAs, such as CRNDE (colorectal neoplasia differentially expressed) and IRAIN (IGF1R antisense imprinted non-protein coding RNA) are associated with the regulation of one single miRNA. However, an increasing number of studies in MM are showing that lncRNAs can regulate or can be regulated by more than one miRNA, such as H19 (H19 imprinted maternally expressed transcript), UCA1 (urothelial cancer associated 1) or OIP5-AS1 (OIP5 antisense RNA 1). Remarkably, there are cases like TUG1 (taurine up-regulated 1) and H19 that are associated with the regulation of the same miRNA, miR-29b-3p (Table 1) [34][40][43][45][46][52][54][58][59][60][61][72][81][82][83][88][90][91][94][95][96]. These results highlight the relevance of the miRNA sponge function of lncRNAs in MM.

Different studies have revealed how the knockdown or upregulation of certain lncRNAs is also associated with different biological and phenotypic effects in MM cells, such as the decrease in cell proliferation or viability, the decrease in cellular migration, the increase in cellular apoptosis and cell cycle arrest (Table 1).

Furthermore, various studies have demonstrated the in vivo biological effect of lncRNA knockdown in MM. For example, the inhibition of DARS-AS1 (DARS antisense RNA 1) or LINC00152 reduces the tumorigenesis of MM cells, whilst the knockdown of SOX2OT (SOX2 overlapping transcript) reduces tumor growth. Moreover, the knockdown of LINC01234 increases miR-124-3p and suppresses GRB2 expression, resulting in a decrease of cell proliferation and the inhibition of MM growth. These results demonstrate that lncRNAs play an important role in the pathobiology of MM (Table 1) [13][34][35][36][40][41][42][43][44][45][46][49][51][52][54][57][58][59][60][63][70][72][78][79][81][82][83][84][85][86][88][90][91][92][94][95][96][97][107].

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