We are analyzing https://link.springer.com/article/10.1186/s12935-021-01912-0.

Title:
LINC01783 facilitates cell proliferation, migration and invasion in non-small cell lung cancer by targeting miR-432-5p to activate the notch pathway | Cancer Cell International
Description:
Background Non-small cell lung cancer (NSCLC) is a common malignancy around the globe. Increasing long non-coding RNAs (lncRNAs) have been confirmed to be associated with the progression of cancers, including NSCLC. Long intergenic non-protein coding RNA 1783 (LINC01783) is a novel lncRNA and its regulatory function as competing endogenous RNA (ceRNA) has not been studied in NSCLC. Methods RT-qPCR measured the expression level of LINC01783 in NSCLC cells. CCK-8, EdU, transwell and wound healing assays were conducted to detect cell proliferation, migration and invasion in NSCLC. The relationship between miR-432-5p and LINC01783 along with delta like 1 (DLL-1) was illustrated by RNA pull down, RIP and luciferase reporter assays. Results LINC01783 was found remarkably increased in NSCLC cell lines, and down-regulation of LINC01783 suppressed cell proliferation, migration and invasion. Then, we discovered Notch pathway was related to the progression of NSCLC, and DLL-1 expression was reduced by LINC01783 knockdown. Furthermore, DLL-1 overexpression could counteract the suppressive effects of LINC01783 down-regulation on the growth of NSCLC cells. MiR-432-5p was observed to be the mutual miRNA that could bind with both LINC01783 and DLL-1. Overexpression of miR-432-5p inhibited DLL-1 expression. In the rescue assays, miR-432-5p depletion offset the impacts of LINC01783 knockdown, and then DLL-1 silence recovered the influence of miR-432-5p down-regulation on NSCLC cell growth. Conclusion LINC01783 aggravates NSCLC cell growth by regulating Notch pathway and sponging miR-432-5p, being a potential target in the treatment for NSCLC.
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Keywords {🔍}

linc, nsclc, cell, cells, cancer, mirp, dll, assays, article, lung, ncih, expression, fig, google, scholar, migration, pathway, rna, notch, proliferation, luciferase, assay, long, progression, conducted, noncoding, reporter, data, transwell, anova, cas, shlinc, invasion, nonsmall, rnas, rtqpcr, knockdown, promotes, usa, cck, wound, sponging, activity, additional, oneway, function, targeting, lncrnas, lncrna, cerna,

Topics {✒️}

bio-mir-432-5p-wt precipitated enrichment triple-negative breast cancer linc01503/mir-342-3p facilitates malignancy mir-520c-3p/s100a4 axis linc00668/mir-432-5p/emt axis suppresses epithelial-mesenchymal transition targeting mir-199b-5p/gbp1 [13] regulating mir-199b-5p/gbp1 targeting mir-16-5p/arpp19 axis rbp-jκ reporter kit rbp-jκ luciferase activity linc01783/mir-432-5p/dll-1 axis dll-1-3′utr-wt luciferase activity fam83h-as1 contributed beas-2b cell line real-world treatment patterns targeting mir-637/ring1 axis lack protein-coding capacities mir-136-5p/metadherin axis sponging mir-520c-3p sponging mir-199b-5p article download pdf cancer-related death cases enhance mir-432-5p expression sponging mir-520a-3p linc01783 modulates mir-432-5p nude mice model post-transcription requires lncrna mir-432-5p significantly impaired targeting mir-432-5p/dll-1 mir-432-5p depletion offset dlx6-as1 accelerated linc01783 targets mir-432-5p promotes cell proliferation mir-143-3p article 31 notch pathway-related proteins lncrna snhg16 promotes mir-143/hk2 axis privacy choices/manage cookies linc01783-specific fish probes nude mice injected cell physiol biochem mir-520a-3p [18] detect cell proliferation detecting cell proliferation cell death dis luciferase reporter assay short noncoding rnas targeting mir-432-5p main treatment methods

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WebPage:
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         headline:LINC01783 facilitates cell proliferation, migration and invasion in non-small cell lung cancer by targeting miR-432-5p to activate the notch pathway
         description:Non-small cell lung cancer (NSCLC) is a common malignancy around the globe. Increasing long non-coding RNAs (lncRNAs) have been confirmed to be associated with the progression of cancers, including NSCLC. Long intergenic non-protein coding RNA 1783 (LINC01783) is a novel lncRNA and its regulatory function as competing endogenous RNA (ceRNA) has not been studied in NSCLC. RT-qPCR measured the expression level of LINC01783 in NSCLC cells. CCK-8, EdU, transwell and wound healing assays were conducted to detect cell proliferation, migration and invasion in NSCLC. The relationship between miR-432-5p and LINC01783 along with delta like 1 (DLL-1) was illustrated by RNA pull down, RIP and luciferase reporter assays. LINC01783 was found remarkably increased in NSCLC cell lines, and down-regulation of LINC01783 suppressed cell proliferation, migration and invasion. Then, we discovered Notch pathway was related to the progression of NSCLC, and DLL-1 expression was reduced by LINC01783 knockdown. Furthermore, DLL-1 overexpression could counteract the suppressive effects of LINC01783 down-regulation on the growth of NSCLC cells. MiR-432-5p was observed to be the mutual miRNA that could bind with both LINC01783 and DLL-1. Overexpression of miR-432-5p inhibited DLL-1 expression. In the rescue assays, miR-432-5p depletion offset the impacts of LINC01783 knockdown, and then DLL-1 silence recovered the influence of miR-432-5p down-regulation on NSCLC cell growth. LINC01783 aggravates NSCLC cell growth by regulating Notch pathway and sponging miR-432-5p, being a potential target in the treatment for NSCLC.
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      headline:LINC01783 facilitates cell proliferation, migration and invasion in non-small cell lung cancer by targeting miR-432-5p to activate the notch pathway
      description:Non-small cell lung cancer (NSCLC) is a common malignancy around the globe. Increasing long non-coding RNAs (lncRNAs) have been confirmed to be associated with the progression of cancers, including NSCLC. Long intergenic non-protein coding RNA 1783 (LINC01783) is a novel lncRNA and its regulatory function as competing endogenous RNA (ceRNA) has not been studied in NSCLC. RT-qPCR measured the expression level of LINC01783 in NSCLC cells. CCK-8, EdU, transwell and wound healing assays were conducted to detect cell proliferation, migration and invasion in NSCLC. The relationship between miR-432-5p and LINC01783 along with delta like 1 (DLL-1) was illustrated by RNA pull down, RIP and luciferase reporter assays. LINC01783 was found remarkably increased in NSCLC cell lines, and down-regulation of LINC01783 suppressed cell proliferation, migration and invasion. Then, we discovered Notch pathway was related to the progression of NSCLC, and DLL-1 expression was reduced by LINC01783 knockdown. Furthermore, DLL-1 overexpression could counteract the suppressive effects of LINC01783 down-regulation on the growth of NSCLC cells. MiR-432-5p was observed to be the mutual miRNA that could bind with both LINC01783 and DLL-1. Overexpression of miR-432-5p inhibited DLL-1 expression. In the rescue assays, miR-432-5p depletion offset the impacts of LINC01783 knockdown, and then DLL-1 silence recovered the influence of miR-432-5p down-regulation on NSCLC cell growth. LINC01783 aggravates NSCLC cell growth by regulating Notch pathway and sponging miR-432-5p, being a potential target in the treatment for NSCLC.
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         Non-small cell lung cancer
         Cancer Research
         Cell Biology
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