ArticleCell death discovery2023
LINC02015 modulates the cell proliferation and apoptosis of aortic vascular smooth muscle cells by transcriptional regulation and protein interaction network.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
2 citing papers in PubMed, 1 citations in OpenAlex.
- LINC02178 drives lung adenocarcinoma progression and serves as a therapeutic target for nanodelivery-based intervention.Scientific reports · 2025Article
- Construction of a Prognostic Model for Cervical Cancer Related to lncRNA Based on Differential Co-expression Network and Functional Study of Key Gene EGFR-AS1.Journal of Cancer · 2025Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Long intergenic nonprotein coding RNA 2015 (LINC02015) is a long non-coding RNA that has been found elevated in various cell proliferation-related diseases. However, the functions and interactive mechanism of LINC02015 remain unknown. This study aimed to explore the role of LINC02015 in the cell proliferation and apoptosis of vascular smooth muscle cells (VSMCs) to explain the pathogenesis of aortic diseases. Ascending aorta samples and angiotensin-II (AT-II) treated primary human aortic VSMCs (HAVSMCs) were used to evaluate the LINC02015 expression. RNA sequencing, chromatin isolation by RNA purification sequencing, RNA pull-down, and mass spectrometry (MS) were applied to explore the potential interacting mechanisms. LINC02015 expression was found elevated in aortic dissection and AT-II-treated HAVSMCs. Cell proliferation and cell cycle were activated in HAVSMCs with LINC02015 knockdown. The cyclins family and caspase family were found to participate in regulating the cell cycle and apoptosis via the NF-κB signaling pathway. RXRA was discovered as a possible hub gene for LINC02015 transcriptional regulating networks. Besides, the protein interaction network of LINC02015 was revealed with candidate regulating molecules. It was concluded that the knockdown of LINC02015 could promote cell proliferation and inhibit the apoptosis of HAVSMCs through an RXRA-related transcriptional regulation network, which could provide a potential therapeutic target for aortic diseases.
Identifiers
What Socratic holds
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 Socratic graph.