Deleted in lymphocytic leukemia 2 (DLEU2): An lncRNA with dissimilar roles in different cancers

Ghafouri‐Fard, Soudeh; Dashti, Sepideh; Farsi, Molood; Taheri, Mohammad

doi:10.1016/j.biopha.2020.111093

Cited by 12 publications

(14 citation statements)

References 18 publications

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“…Furthermore, among our top predicted proliferation/growth inducers were the lncRNAs DLEU2, TMPO-AS1 , and MIR17HG . DLEU2 has been verified as a proliferation-inducing lncRNA in the vast majority of cancer types (13 out of 16) ( Ghafouri-Fard et al, 2021 ), and TMPO-AS1 has a role in tumorigenesis and progression and is overexpressed in 15 different cancer types ( Zheng et al, 2021 ). The lncRNA MIR17HG is the host gene of the miR-17–92 cluster, which consists of a group of onco-microRNAs that induce pan-cancer cell proliferation/growth ( Mogilyansky and Rigoutsos, 2013 ).…”

Section: Resultsmentioning

confidence: 99%

Systematic lncRNA mapping to genome-wide co-essential modules uncovers cancer dependency on uncharacterized lncRNAs

Mitra

Adams

Eischen

2022

eLife

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Quantification of gene dependency across hundreds of cell lines using genome-scale CRISPR screens has revealed co-essential pathways/modules and critical functions of uncharacterized genes. In contrast to protein-coding genes, robust CRISPR-based loss-of-function screens are lacking for long noncoding RNAs (lncRNAs), which are key regulators of many cellular processes, leaving many essential lncRNAs unidentified and uninvestigated. Integrating copy number, epigenetic, and transcriptomic data of >800 cancer cell lines with CRISPR-derived co-essential pathways, our method recapitulates known essential lncRNAs and predicts proliferation/growth dependency of 289 poorly characterized lncRNAs. Analyzing lncRNA dependencies across 10 cancer types and their expression alteration by diverse growth inhibitors across cell types, we prioritize 30 high-confidence pan-cancer proliferation/growth-regulating lncRNAs. Further evaluating two previously uncharacterized top proliferation-suppressive lncRNAs (PSLR-1, PSLR-2) showed they are transcriptionally regulated by p53, induced by multiple cancer treatments, and significantly correlate to increased cancer patient survival. These lncRNAs modulate G2 cell cycle-regulating genes within the FOXM1 transcriptional network, inducing a G2 arrest and inhibiting proliferation and colony formation. Collectively, our results serve as a powerful resource for exploring lncRNA-mediated regulation of cellular fitness in cancer, circumventing current limitations in lncRNA research.

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Section: Resultsmentioning

confidence: 99%

Systematic lncRNA mapping to genome-wide co-essential modules uncovers cancer dependency on uncharacterized lncRNAs

Mitra

Adams

Eischen

2022

eLife

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“…Another study reported that LOC541471 is a novel prognostic biomarker for head and neck squamous cell carcinoma [ 38 ]. The leukaemia 2 gene (DLEU2) has been reported to play an important role in a variety of diseases [ 39 , 40 ], especially in tumour diseases, including thyroid cancer, gastric cancer, sarcopenia, and laryngeal squamous cell carcinoma, and has been shown to play a role through the ceRNA mechanism [ 41 – 44 ].…”

Section: Resultsmentioning

confidence: 99%

Comprehensive analysis of the long noncoding RNA-associated competitive endogenous RNA network in the osteogenic differentiation of periodontal ligament stem cells

Lai¹,

Wang

Qiu

et al. 2022

BMC Genomics

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Backgroud The mechanism implicated in the osteogenesis of human periodontal ligament stem cells (PDLSCs) has been investigated for years. Previous genomics data analyses showed that long noncoding RNA (lncRNA), microRNA (miRNA) and messenger RNA (mRNA) have significant expression differences between induced and control human PDLSCs. Competing for endogenous RNAs (ceRNA), as a widely studied mechanism in regenerative medicine, while rarely reported in periodontal regeneration. The key lncRNAs and their ceRNA network might provide new insights into molecular therapies of periodontal regeneration based on PDLSCs. Results Two networks reflecting the relationships among differentially expressed RNAs were constructed. One ceRNA network was composed of 6 upregulated lncRNAs, 280 upregulated mRNAs, and 18 downregulated miRNAs. The other network contained 33 downregulated lncRNAs, 73 downregulated mRNAs, and 5 upregulated miRNAs. Functional analysis revealed that 38 GO terms and 8 pathways related with osteogenesis were enriched. Twenty-four osteogenesis-related gene-centred lncRNA-associated ceRNA networks were successfully constructed. Among these pathways, we highlighted MAPK and TGF-beta pathways that are closely related to osteogenesis. Subsequently, subnetworks potentially linking the GO:0001649 (osteoblast differentiation), MAPK and TGF-beta pathways were constructed. The qRT-PCR validation results were consistent with the microarray analysis. Conclusion We construct a comprehensively identified lncRNA-associated ceRNA network might be involved in the osteogenesis of PDLSCs, which could provide insights into the regulatory mechanisms and treatment targets of periodontal regeneration.

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“…Furthermore, among our top predicted proliferation/growth inducers were the lncRNAs DLEU2 , TMPO-AS1 , and MIR17HG . DLEU2 has been verified as a proliferation-inducing lncRNA in the vast majority of cancer types (13 out of 16) (Ghafouri-Fard, Dashti, Farsi, & Taheri, 2021), and TMPO-AS1 has a role in tumorigenesis and progression and is overexpressed in 15 different cancer types(Zheng et al, 2021). The lncRNA MIR17HG is the host gene of the miR-17-92 cluster, which consists of a group of onco- microRNAs that induce pan-cancer cell proliferation/growth(Mogilyansky & Rigoutsos, 2013).…”

Section: Resultsmentioning

confidence: 99%

Systematic lncRNA mapping to genome-wide co-essential pathways uncovers cancer dependency on uncharacterized lncRNAs

Mitra

Adams

Eischen

2022

Preprint

View full text Add to dashboard Cite

Quantification of gene dependency across hundreds of cell lines using genome-scale CRISPR screens have revealed co-essential pathways/modules and critical functions of uncharacterized genes. In contrast to protein-coding genes, robust CRISPR-based loss-of-function screens are lacking for long non-coding RNAs (lncRNAs), which are key regulators of many cellular process, leaving many essential lncRNAs unidentified and uninvestigated. Integrating copy-number, epigenetic, and transcriptomic data of >800 cancer cell lines with CRISPR-derived co-essential pathways, our method recapitulates known essential lncRNAs and predicts proliferation/growth dependency of 289 poorly characterized lncRNAs. Analyzing lncRNA dependencies across ten cancer types and their expression alteration by diverse growth-inhibitors across cell types, we prioritize 30 high-confidence pan-cancer proliferation/growth-regulating lncRNAs. Further evaluating two previously uncharacterized top proliferation suppressive lncRNAs (PSLR-1, PSLR-2) showed they are transcriptionally regulated by p53, induced by multiple cancer treatments, and significantly correlate to increased cancer patient survival. These lncRNAs modulate G2 cell cycle-regulating genes within the FOXM1 transcriptional network, inducing a G2 arrest and inhibiting proliferation and colony formation. Collectively, our results serve as a powerful resource for exploring lncRNA-mediated regulation of cellular fitness in cancer, circumventing current limitations in lncRNA research.

show abstract

Deleted in lymphocytic leukemia 2 (DLEU2): An lncRNA with dissimilar roles in different cancers

Cited by 12 publications

References 18 publications

Systematic lncRNA mapping to genome-wide co-essential modules uncovers cancer dependency on uncharacterized lncRNAs

Systematic lncRNA mapping to genome-wide co-essential modules uncovers cancer dependency on uncharacterized lncRNAs

Comprehensive analysis of the long noncoding RNA-associated competitive endogenous RNA network in the osteogenic differentiation of periodontal ligament stem cells

Systematic lncRNA mapping to genome-wide co-essential pathways uncovers cancer dependency on uncharacterized lncRNAs

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