Expression and functions of long non-coding RNA NEAT1 and isoforms in breast cancer

Knutsen, Erik; Harris, Adrian L.; Perander, Maria

doi:10.1038/s41416-021-01588-3

Cited by 34 publications

(23 citation statements)

References 144 publications

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“…This suggests the NFkB regulation by TNF as a transcriptomic hallmark common to a subset of resistant and sensitive luminal cells. Cell cluster_5 is also significantly associated to the lncRNA-Topic 13, which includes MALAT1 and NEAT1 as top ranked non coding genes, two lncRNAs extensively studied in breast cancer progression (23)(24). Another important result shows the association of cluster_6 composed only of therapy-resistant luminal cells, to mRNA-Topic 12 (HALLMARK_EPITHELIAL_MESENCHYMAL_TRANSITION) and lncRNA-Topic 19 (lncRNAs in chromatin accessible regions of IPC cells).…”

Section: Resultsmentioning

confidence: 99%

Identification of interpretable clusters and associated signatures in breast cancer single cell data: a topic modeling approach

Malagoli

Valle

Barillot

et al. 2022

Preprint

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Single-cell RNA sequencing is a powerful tool to explore cancer heterogeneity. However, the expression of lncRNAs in single cells is still to be studied extensively and methods to deal with the sparsity of this type of data are lacking. Here, we propose a topic modeling approach to investigate the transcriptional heterogeneity of luminal and triple negative breast cancer cells using patient-derived xenograft models of acquired resistance to chemotherapy and targeted therapy. We show that using an integrative clustering that combines the information coming from mRNAs and lncRNAs treated as disjoint omic layers greatly improves the accuracy of cell classification. Topics associated with specific breast cancer subpopulations show a clear enrichment for pathways involved in subtyping and progression of breast cancer and to sets of lncRNA encoded in the open chromatin regions of breast cancer cell lines. We identified lncRNAs strongly associated with cell clusters already well known in the literature, such as MALAT1 and NEAT1, and highlighted some others that may be clinically relevant.

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Section: Resultsmentioning

confidence: 99%

Identification of interpretable clusters and associated signatures in breast cancer single cell data: a topic modeling approach

Malagoli

Valle

Barillot

et al. 2022

Preprint

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“…However, NEAT1.1 containing with only two domains for RNA stability and isoform selection seems to have contributed less to paraspeckle formation. The mechanism behind the opposite effects on tumor of NEAT1.1 and NEAT1.2 still remain obscure [13]. According to previous studies of the same kind non-coding RNAs in nucleus [14,15], lncRNA could facilitate the connection between transcription factors or epigenetic regulators and DNA elements.…”

Section: Discussionmentioning

confidence: 99%

NEAT1 variant 1 weakens the genome-wide effect of miR-3122 on blocking H3K79me3 in bladder cancer

Zhao

Sun

Zhang

et al. 2022

Aging

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Nuclear-enriched abundant transcript 1 (NEAT1) is one of the most well-studied long non-coding RNAs (lncRNAs) in multiple human carcinoma. Two distinct variants of NEAT1, however, are never illuminated their specific functions and mechanisms underlying carcinogenesis. In this study, biotin-labelled NEAT1 variants were generated to incubate with cell lysate of bladder cancer cell T24 cells, and fished a batch of RNA substances. Here, we observed that NEAT1.1 (the short transcript) could capture 122 microRNAs (miRNAs), 36 small nucleolar RNAs (snoRNAs), 55 lncRNAs and 38 mRNAs while NEAT1.2 (the long transcript) could obtain 142 miRNAs, 51 snoRNAs, 72 lncRNAs and 41 mRNAs. Furthermore, we also found that the distinctions of RNA binding substances between these two variants were mainly expressed in nucleus rather than cytoplasm. GO analysis indicated that these non-coding RNAs governed histone modification, nucleosome assembly and chromosome organization. We picked up miRNA miR-3122, which substantially interacted with NEAT1.1, and found that histone H3K79me3 was reduced in bladder cancer T24, BIU-87 and EJ-1 cells after miR-3122 overexpression, and rescued by NEAT1.1 additional compensation. Nonetheless, we failed to find that miR-3122 could interfere with expression of H3K79 methyltransferase disruptor of telomeric silencing-1 like (DOT1L). Interestingly, we harvested histone 3 fished by biotin-labelled miR-3122, and validated this intercrossing using RNA immunoprecipitation. Taken together, we demonstrated that NEAT1.1 weakened the effect of miR-3122 on H3K79me3 suppression in bladder cancer.

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“…It has already been established that lncRNAs are important regulators and control complex cellular behavior in breast cancer [35][36][37], which has received much attention from several researchers. Based on the importance of lncRNAs in breast cancer, identifying novel breast cancer-related lncRNAs and elucidating their functions in tumorigenesis are of great value.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA PPP1R14B-AS1 imitates microRNA-134-3p to facilitate breast cancer progression by upregulating LIM and SH3 protein 1

ZHOU¹,

ZHANG²,

Guan³

et al. 2021

Oncology Research

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Long noncoding RNA PPP1R14B antisense RNA 1 (PPP1R14B-AS1) has emerged as a critical modulator of liver cancer and lung adenocarcinoma progression. However, the functional importance and biological relevance of PPP1R14B-AS1 in breast cancer remain unclear. Therefore, this study was designed to detect PPP1R14B-AS1 levels in breast cancer cells using qRT-PCR and elucidate the influence of PPP1R14B-AS1 on aggressive phenotypes.Furthermore, molecular events mediating the action of PPP1R14B-AS1 were characterized in detail. Functional experiments addressed the impacts of PPP1R14B-AS1 knockdown on breast cancer cells. In this study, PPP1R14B-AS1 was found to be overexpressed in breast cancer, exhibiting a close correlation with poor patient prognosis.Results also showed that breast cancer cell proliferation and motility were suppressed when PPP1R14B-AS1 was silenced. Mechanistically, PPP1R14B-AS1 acted as a competing endogenous RNA for microRNA-134-3p (miR-134-3p) in breast cancer cells. PPP1R14B-AS1 also increased LIM and SH3 protein 1 (LASP1) levels by imitating miR-134-3p in breast cancer cells. Rescue experiments further corroborated that the knockdown of miR-134-3p or an increase in LASP1 restored the aggressive malignant characteristics of breast cancer cells that were weakened by PPP1R14B-AS1 depletion. In summary, PPP1R14B-AS1 facilitated the oncogenicity of breast cancer cells by controlling the miR-134-3p/LASP1 axis. We believe that our findings may contribute to the development of precision therapy techniques in the field of breast cancer treatment.

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Expression and functions of long non-coding RNA NEAT1 and isoforms in breast cancer

Cited by 34 publications

References 144 publications

Identification of interpretable clusters and associated signatures in breast cancer single cell data: a topic modeling approach

Identification of interpretable clusters and associated signatures in breast cancer single cell data: a topic modeling approach

NEAT1 variant 1 weakens the genome-wide effect of miR-3122 on blocking H3K79me3 in bladder cancer

Long noncoding RNA PPP1R14B-AS1 imitates microRNA-134-3p to facilitate breast cancer progression by upregulating LIM and SH3 protein 1

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