Probes for INS
ACD can configure probes for the various manual and automated assays for INS for RNAscope Assay, or for Basescope Assay compatible for your species of interest.
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Cells
2022 May 03
Pellegrino, R;Castoldi, M;Ticconi, F;Skawran, B;Budczies, J;Rose, F;Schwab, C;Breuhahn, K;Neumann, UP;Gaisa, NT;Loosen, SH;Luedde, T;Costa, IG;Longerich, T;
PMID: 35563834 | DOI: 10.3390/cells11091528
Genomic and epigenomic studies revealed dysregulation of long non-coding RNAs in many cancer entities, including liver cancer. We identified an epigenetic mechanism leading to upregulation of the long intergenic non-coding RNA 152 (LINC00152) expression in human hepatocellular carcinoma (HCC). Here, we aimed to characterize a potential competing endogenous RNA (ceRNA) network, in which LINC00152 exerts oncogenic functions by sponging miRNAs, thereby affecting their target gene expression. Database and gene expression data of human HCC were integrated to develop a potential LINC00152-driven ceRNA in silico. RNA immunoprecipitation and luciferase assay were used to identify miRNA binding to LINC00152 in human HCC cells. Functionally active players in the ceRNA network were analyzed using gene editing, siRNA or miRNA mimic transfection, and expression vectors in vitro. RNA expression in human HCC in vivo was validated by RNA in situ hybridization. Let-7c-5p, miR-23a-3p, miR-125a-5p, miR-125b-5p, miR-143a-3p, miR-193-3p, and miR-195-5p were detected as new components of the potential LINC00152 ceRNA network in human HCC. LINC00152 was confirmed to sponge miR143a-3p in human HCC cell lines, thereby limiting its binding to their respective target genes, like KLC2. KLC2 was identified as a central mediator promoting pro-tumorigenic effects of LINC00152 overexpression in HCC cells. Furthermore, co-expression of LINC00152 and KLC2 was observed in human HCC cohorts and high KLC2 expression was associated with shorter patient survival. Functional assays demonstrated that KLC2 promoted cell proliferation, clonogenicity and migration in vitro. The LINC00152-miR-143a-3p-KLC2 axis may represent a therapeutic target in human HCC.
EMBO reports
2022 Dec 16
Wang, B;Jiang, B;Li, GW;Dong, F;Luo, Z;Cai, B;Wei, M;Huang, J;Wang, K;Feng, X;Tong, F;Wang, S;Wang, Q;Han, Q;Li, C;Zhang, X;Yang, L;Bao, L;
PMID: 36524339 | DOI: 10.15252/embr.202154313
Somatosensory neurons are highly heterogeneous with distinct types of neural cells responding to specific stimuli. However, the distribution and roles of cell-type-specific long intergenic noncoding RNAs (lincRNAs) in somatosensory neurons remain largely unexplored. Here, by utilizing droplet-based single-cell RNA-seq (scRNA-seq) and full-length Smart-seq2, we show that lincRNAs, but not coding mRNAs, are enriched in specific types of mouse somatosensory neurons. Profiling of lincRNAs from single neurons located in dorsal root ganglia (DRG) identifies 200 lincRNAs localized in specific types or subtypes of somatosensory neurons. Among them, the conserved cell-type-specific lincRNA CLAP associates with pruritus and is abundantly expressed in somatostatin (SST)-positive neurons. CLAP knockdown reduces histamine-induced Ca2+ influx in cultured SST-positive neurons and in vivo reduces histamine-induced scratching in mice. In vivo knockdown of CLAP also decreases the expression of neuron-type-specific and itch-related genes in somatosensory neurons, and this partially depends on the RNA binding protein MSI2. Our data reveal a cell-type-specific landscape of lincRNAs and a function for CLAP in somatosensory neurons in sensory transmission.
Basic research in cardiology
2023 Jan 26
Boos, F;Oo, JA;Warwick, T;Günther, S;Izquierdo Ponce, J;Lopez, M;Rafii, D;Buchmann, G;Pham, MD;Msheik, ZS;Li, T;Seredinski, S;Haydar, S;Kashefiolasl, S;Plate, KH;Behr, R;Mietsch, M;Krishnan, J;Pullamsetti, SS;Bibli, SI;Hinkel, R;Baker, AH;Boon, RA;Schulz, MH;Wittig, I;Miller, FJ;Brandes, RP;Leisegang, MS;
PMID: 36700983 | DOI: 10.1007/s00395-023-00978-3
Long non-coding RNAs (lncRNAs) can act as regulatory RNAs which, by altering the expression of target genes, impact on the cellular phenotype and cardiovascular disease development. Endothelial lncRNAs and their vascular functions are largely undefined. Deep RNA-Seq and FANTOM5 CAGE analysis revealed the lncRNA LINC00607 to be highly enriched in human endothelial cells. LINC00607 was induced in response to hypoxia, arteriosclerosis regression in non-human primates, post-atherosclerotic cultured endothelial cells from patients and also in response to propranolol used to induce regression of human arteriovenous malformations. siRNA knockdown or CRISPR/Cas9 knockout of LINC00607 attenuated VEGF-A-induced angiogenic sprouting. LINC00607 knockout in endothelial cells also integrated less into newly formed vascular networks in an in vivo assay in SCID mice. Overexpression of LINC00607 in CRISPR knockout cells restored normal endothelial function. RNA- and ATAC-Seq after LINC00607 knockout revealed changes in the transcription of endothelial gene sets linked to the endothelial phenotype and in chromatin accessibility around ERG-binding sites. Mechanistically, LINC00607 interacted with the SWI/SNF chromatin remodeling protein BRG1. CRISPR/Cas9-mediated knockout of BRG1 in HUVEC followed by CUT&RUN revealed that BRG1 is required to secure a stable chromatin state, mainly on ERG-binding sites. In conclusion, LINC00607 is an endothelial-enriched lncRNA that maintains ERG target gene transcription by interacting with the chromatin remodeler BRG1 to ultimately mediate angiogenesis.
Clinical science (London, England : 1979)
2023 Jan 27
Yiu, WH;Lok, SW;Xue, R;Chen, J;Lai, KN;Lan, HY;Tang, SC;
PMID: 36705251 | DOI: 10.1042/CS20220537
Kidney inflammation contributes to the progression of chronic kidney disease (CKD). Modulation of Toll-like receptor 4 (TLR4) signaling is a potential therapeutic strategy for this pathology, but the regulatory mechanisms of TLR4 signaling in kidney tubular inflammation remains unclear. Here, we demonstrated that tubule-specific deletion of TLR4 in mice conferred protection against obstruction-induced kidney injury, with reduction in inflammatory cytokine production, macrophage infiltration and kidney fibrosis. Transcriptome analysis revealed a marked downregulation of long noncoding RNA (lncRNA) Meg3 in the obstructed kidney from tubule-specific TLR4 knockout mice compared to wild type control. Meg3 was also induced by LPS in tubular epithelial cells via a p53-dependent signaling pathway. Silencing of Meg3 suppressed LPS-induced cytokine production of CCL-2 and CXCL-2 and the activation of p38 MAPK pathway in vitro and ameliorated kidney fibrosis in mice with obstructive nephropathy. Together, these findings identify a proinflammatory role of lncRNA Meg3 in CKD and suggest a novel regulatory pathway in TLR4-driven inflammatory responses in tubular epithelial cells.
Cell death & disease
2023 Feb 22
Duan, Y;Yue, K;Ye, B;Chen, P;Zhang, J;He, Q;Wu, Y;Lai, Q;Li, H;Wu, Y;Jing, C;Wang, X;
PMID: 36813772 | DOI: 10.1038/s41419-023-05667-6
Long non-coding RNAs (LncRNAs) are implicated in malignant progression of human cancers. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a well-known lncRNA, has been reported to play crucial roles in multiple malignancies including head and neck squamous cell carcinoma (HNSCC). However, the underlying mechanisms of MALAT1 in HNSCC progression remain to be further investigated. Here, we elucidated that compared with normal squamous epithelium, MALAT1 was notably upregulated in HNSCC tissues, especially in which was poorly differentiated or with lymph nodes metastasis. Moreover, elevated MALAT1 predicted unfavorable prognosis of HNSCC patients. The results of in vitro and in vivo assays showed that targeting MALAT1 could significantly weaken the capacities of proliferation and metastasis in HNSCC. Mechanistically, MALAT1 inhibited von Hippel-Lindau tumor suppressor (VHL) by activating EZH2/STAT3/Akt axis, then promoted the stabilization and activation of β-catenin and NF-κB which could play crucial roles in HNSCC growth and metastasis. In conclusion, our findings reveal a novel mechanism for malignant progression of HNSCC and suggest that MALAT1 might be a promising therapeutic target for HNSCC treatment.
Cancer immunology research
2022 Jul 21
Yu, H;Chen, C;Han, F;Tang, J;Deng, M;Niu, Y;Lai, M;Zhang, H;
PMID: 35862232 | DOI: 10.1158/2326-6066.CIR-21-1011
MIR4435-2HG, also known as LINC00978, has previously been described as an oncogenic long noncoding RNA (lncRNA). However, we show here that Mir4435-2hg depletion promoted colorectal tumorigenesis and progression in in vivo models of colitis-associated colorectal cancer (CRC), spontaneous intestinal adenomatous polyposis, and subcutaneous tumors. Alteration of MIR4435-2HG in CRC cells did not change the potential for cell proliferation, migration, or invasion in vitro. RNAscope assays showed that most MIR4435-2HG was located in the tumor stroma, which caused high expression of MIR4435-2HG in CRC tumor tissue. Transcriptome analysis of CRC tissues from wild-type and Mir4435-2hg-deficient mice revealed Mir4435-2hg as a tumor suppressor gene that regulated the immune microenvironment. Loss of Mir4435-2hg led to a decline in neutrophils and elevation of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs). In tissue-specific Mir4435-2hg knockout mice, we confirmed that Mir4435-2hg depletion in neutrophils, but not in intestinal epithelial cells, promoted CRC progression. Mechanistically, Mir4435-2hg depletion enhanced the immunosuppressive ability of PMN-MDSCs by disturbing their fatty acid metabolism. These findings suggest that MIR4435-2HG is a tumor-suppressing lncRNA whose deficiency could increase tumor-infiltrating PMN-MDSCs and enhance the immunosuppressive potential of PMN-MDSCs to promote CRC development. This provides a theoretical basis for further illustrating the pathogenesis of CRC and a potential antitumor immunotherapy target.
Annals of Gastroenterological Surgery
2022 Dec 29
Ichihara, M;Takahashi, H;Nishida, N;Ivan, C;Okuzaki, D;Yokoyama, Y;Ohtsuka, M;Miyoshi, N;Uemura, M;Tanaka, S;Calin, G;Mori, M;Doki, Y;Eguchi, H;Yamamoto, H;
| DOI: 10.1002/ags3.12649
Background Studies have shown that cancer stemness and the endoplasmic reticulum (ER) stress response are inversely regulated in colorectal cancer (CRC), but the mechanism has not been fully clarified. Long noncoding RNAs (lncRNAs) play key roles in cancer progression and metastasis. In this study we investigated lncRNA 01534 (LINC01534) as a possible modulator between cancer stemness and ER stress response. Methods In vitro experiments using CRC cell lines were performed to explore a possible role of LINC01534. The expression of LINC01534 in clinical CRC samples was assessed by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and in situ hybridization. Results Silencing LINC01534 led to suppression of cell proliferation, invasiveness, and cell cycle progression at the G2-M phase, and promoted apoptosis. Moreover, we found that silencing LINC01534 suppressed cancer stemness, while it activated the ER stress response, especially through the PERK/eIF2α signaling pathway. In situ hybridization revealed LINC01534 was expressed in tumor cells and upregulated in CRC tissues compared with normal epithelium. A survival survey indicated that high LINC01534 expression was significantly associated with shorter overall survival in 187 CRC patients. Conclusion This is the first report on LINC01534 in human cancer. Our findings suggest that LINC01534 may be an important modulator of the maintenance of cancer stemness and suppression of the ER stress response, and that it could be a novel prognostic factor in CRC.
JACC: Basic to Translational Science
2022 Sep 01
Chen, L;Liu, H;Sun, C;Pei, J;Li, J;Li, Y;Wei, K;Wang, X;Wang, P;Li, F;Gai, S;Zhao, Y;Zheng, Z;
| DOI: 10.1016/j.jacbts.2022.06.009
Based on high-throughput transcriptomic sequencing, SNHG3 was among the most highly expressed long noncoding RNAs in calcific aortic valve disease. SNHG3 upregulation was verified in human and mouse calcified aortic valves. Moreover, in vivo and in vitro studies showed SNHG3 silencing markedly ameliorated aortic valve calcification. In-depth functional assays showed SNHG3 physically interacted with polycomb repressive complex 2 to suppress the H3K27 trimethylation BMP2 locus, which in turn activated BMP2 expression and signaling pathways. Taken together, SNHG3 promoted aortic valve calcification by upregulating BMP2, which might be a novel therapeutic target in human calcific aortic valve disease.
The Journal of investigative dermatology
2023 Jan 11
Luo, L;Pasquali, L;Srivastava, A;Freisenhausen, JC;Pivarcsi, A;Sonkoly, E;
PMID: 36641130 | DOI: 10.1016/j.jid.2022.12.011
Psoriasis is a common immune-mediated skin disease characterized by epidermal hyperproliferation and chronic skin inflammation. Long non-coding RNAs (lncRNAs) are >200 nucleotide long transcripts, which possess important regulatory functions. To date, little is known about the contribution of lncRNAs to psoriasis. Here, we identify LINC00958 as a lncRNA overexpressed in keratinocytes from psoriasis skin lesions, in a transcriptomic screen performed on keratinocytes sorted from psoriasis and healthy skin. Increased levels of LINC00958 in psoriasis keratinocytes were confirmed by RT-qPCR and single molecule in situ hybridization. Confocal microscopy and analysis of subcellular fractions showed that LINC00958 is mainly localized in the cytoplasm of keratinocytes. IL-17A, a key psoriasis cytokine, induced LINC00958 in keratinocytes through C/EBP-β and the p38 pathway. Inhibition of LINC00958 led to decreased proliferation as measured by Ki67 expression, IncuCyte imaging and EdU assays. Transcriptomic analysis of LINC00958-depleted keratinocytes revealed enrichment of proliferation and cell cycle-related genes among differentially expressed transcripts. Moreover, LINC00958-depletion led to decreased basal and IL-17A-induced phosphorylation of p38. Furthermore, IL-17A-induced keratinocyte proliferation was counteracted by the inhibition of LINC00958. In summary, our data support a role for the IL-17A-induced lncRNA, LINC00958, in the pathological circuits in psoriasis by reinforcing IL-17A-induced epidermal hyperproliferation.
The American journal of pathology
2022 Dec 10
Su, A;Yao, K;Zhang, H;Wang, Y;Zhang, H;Tang, J;
PMID: 36509121 | DOI: 10.1016/j.ajpath.2022.11.007
An increasing body of evidence suggests that long noncoding RNAs play critical roles in human cancer. Breast cancer is a heterogeneous disease and the potential involvement of long noncoding RNAs in breast cancer remains poorly understood. Herein, researchers identified a long noncoding RNA, DANCR, which promotes cisplatin chemoresistance in triple-negative breast cancer cells. Mechanistically, DANCR could bind to Krüppel-like factor 5 (KLF5) and induce acetylation of KLF5 at lysine 369 (K369), and DANCR knockdown resulted in down-regulation of KLF5 protein levels. Furthermore, researchers found that the DANCR/KLF5 signaling pathway induced hypersensitivity to cisplatin in chemoresistant patients by inhibiting p27 transcription. In summary, researcher's study reinforces the potential presence of a growth regulatory network found in triple-negative breast cancer cells, and a DANCR/KLF5/p27 signaling pathway was documented in the present study that mediates cisplatin chemoresistance in triple-negative breast cancer.
Theriogenology
2023 Jan 10
Zhang, R;Guo, X;Li, H;Li, Z;Gong, S;Li, H;Ma, Y;Liu, H;Gao, C;Wang, A;Jin, Y;Lin, P;
PMID: 36731281 | DOI: 10.1016/j.theriogenology.2023.01.008
Endometrial receptivity is a critical process for the successful establishment of pregnancy in ruminants. However, the biological role of long non-coding RNAs (lncRNAs) in the development of endometrial receptivity is poorly understood. In this study, we performed RNA-seq analysis of immortalised goat endometrial epithelial cells (gEECs) treated with interferon-τ (IFNT). Transcriptome profiles showed that 8069 high-confidence putative lncRNAs, including 6498 intronic lncRNA transcripts, 1078 lincRNAs and 493 antisense lncRNAs were identified in gEECs with or without IFNT treatment. Functional clustering analysis was performed by using cis and trans lncRNAs prediction. GO and KEGG analyses revealed that differentially expressed lncRNAs may regulate tissue remodelling and immune responses. Subsequently, six of the 21 differentially expressed antisense lncRNAs were validated using qRT-PCR. Through functional screening and co-expression analysis of lncRNAs in gEECs, we identified that ISG15-AS was mainly expressed in the luminal and glandular epithelium on days 5 and 15 and was strongly upregulated on day 18 of pregnancy in vivo. Similarly, ISG15-AS was abundant in the nucleus and cytoplasm, and was significantly upregulated after treatment with IFNT in gEECs. In addition, ISG15 is an IFNT-responsive gene, that displayed an evident increase in vivo and in vitro. Moreover, sense ISG15 was significantly upregulated following ISG15-AS silencing. The key genes related to ISGylation and endometrial receptivity in gEECs dramatically increased after ISG15-AS inhibition. Collectively, our results indicate that a novel antisense lncRNA, ISG15-AS, may be important in regulating endometrial receptivity through ISGylation.
Journal of molecular and cellular cardiology
2022 Jun 14
Ding, S;Liu, J;Han, X;Ding, W;Liu, Z;Zhu, Y;Zhan, W;Wan, Y;Gai, S;Hou, J;Wang, X;Wu, Y;Wu, A;Li, CY;Zheng, Z;Tian, XL;Cao, H;
PMID: 35714558 | DOI: 10.1016/j.yjmcc.2022.06.001
Long noncoding RNAs (lncRNAs) are critical regulators of inflammation with great potential as new therapeutic targets. However, the role of lncRNAs in early atherosclerosis remains poorly characterized. This study aimed to identify the key lncRNA players in activated endothelial cells (ECs). The lncRNAs in response to pro-inflammatory factors in ECs were screened through RNA sequencing. ICAM-1-related non-coding RNA (ICR) was identified as the most potential candidate for early atherosclerosis. ICR is essential for intercellular adhesion molecule-1 (ICAM1) expression, EC adhesion and migration. In a high fat diet-induced atherosclerosis model in mice, ICR is upregulated in the development of atherosclerosis. After intravenous injection of adenovirus carrying shRNA for mouse ICR, the atherosclerotic plaque area was markedly reduced with the declined expression of ICR and ICAM1. Mechanistically, ICR stabilized the mRNA of ICAM1 in quiescent ECs; while under inflammatory stress, ICR upregulated ICAM1 in a nuclear factor kappa B (NF-κB) dependent manner. RNA-seq analysis showed pro-inflammatory targets of NF-κB were regulated by ICR. Furthermore, the chromatin immunoprecipitation assays showed that p65 binds to ICR promoter and facilitates its transcription. Interestingly, ICR, in turn, promotes p65 accumulation and activity, forming a positive feedback loop to amplify NF-κB signaling. Preventing the degradation of p65 using proteasome inhibitors rescued the expression of NF-κB targets suppressed by ICR. Taken together, ICR acts as an accelerator to amplify NF-κB signaling in activated ECs and suppressing ICR is a promising early intervention for atherosclerosis through ICR/p65 loop blockade.
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| Description | ||
|---|---|---|
| sense Example: Hs-LAG3-sense | Standard probes for RNA detection are in antisense. Sense probe is reverse complent to the corresponding antisense probe. | |
| Intron# Example: Mm-Htt-intron2 | Probe targets the indicated intron in the target gene, commonly used for pre-mRNA detection | |
| Pool/Pan Example: Hs-CD3-pool (Hs-CD3D, Hs-CD3E, Hs-CD3G) | A mixture of multiple probe sets targeting multiple genes or transcripts | |
| No-XSp Example: Hs-PDGFB-No-XMm | Does not cross detect with the species (Sp) | |
| XSp Example: Rn-Pde9a-XMm | designed to cross detect with the species (Sp) | |
| O# Example: Mm-Islr-O1 | Alternative design targeting different regions of the same transcript or isoforms | |
| CDS Example: Hs-SLC31A-CDS | Probe targets the protein-coding sequence only | |
| EnEm | Probe targets exons n and m | |
| En-Em | Probe targets region from exon n to exon m | |
| Retired Nomenclature | ||
| tvn Example: Hs-LEPR-tv1 | Designed to target transcript variant n | |
| ORF Example: Hs-ACVRL1-ORF | Probe targets open reading frame | |
| UTR Example: Hs-HTT-UTR-C3 | Probe targets the untranslated region (non-protein-coding region) only | |
| 5UTR Example: Hs-GNRHR-5UTR | Probe targets the 5' untranslated region only | |
| 3UTR Example: Rn-Npy1r-3UTR | Probe targets the 3' untranslated region only | |
| Pan Example: Pool | A mixture of multiple probe sets targeting multiple genes or transcripts | |
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