ArticleCell death & disease2021
Novel cytoplasmic lncRNA IKBKBAS promotes lung adenocarcinoma metastasis by upregulating IKKβ and consequential activation of NF-κB signaling pathway.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- The role of long non-coding RNAs in lung cancer metastasis: Molecular mechanisms, pathogenesis and clinical implications.Clinical and translational medicine · 2025Review
- Comprehensive landscape and future perspective of long noncoding RNAs in non-small cell lung cancer: it takes a village.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- Dinuclear gold(I) complexes based on carbene and diphosphane ligands: bis[2-(dicyclohexylphosphano)ethyl]amine complex inhibits the proteasome activity, decreases stem cell markers and spheroid viability in lung cancer cells.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2023Article
- Metabolic heterogeneity in early-stage lung adenocarcinoma revealed by RNA-seq and scRNA-seq.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
NF-κB signaling pathway is a critical link between inflammation and cancer. Emerging evidence suggested that long non-coding RNAs (lncRNAs) were involved in dysregulation of NF-κB. Herein, we reported a novel lncRNA IKBKBAS that activated NF-κB in lung adenocarcinoma (LUAD) by upregulating IKKβ, a key member of NF-κB signaling pathway, thereby promoting the metastasis of LUAD both in vitro and in vivo. The upregulated IKBKBAS functioned as a competing endogenous RNA (ceRNA) via competing with IKKβ mRNA for binding miR-4741, consequently leading to upregulation and activation of IKKβ, and ultimately activation of NF-κB. The abnormally elevated IKBKBAS in LUAD was mainly resulted from the extremely decrease of miR-512-5p that targeting IKBKBAS. Furthermore, we identified a positive feedback loop between NF-κB and IKBKBAS, in which NF-κB activation induced by overexpression of IKBKBAS could promote the transcription of IKBKBAS by binding the κB sites within IKBKBAS promoter. Our studies revealed that IKBKBAS was involved in the activation of NF-κB signaling by upregulating the expression of IKKβ, which made it serve as a potential novel target for therapies to LUAD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.