ArticleBMC pulmonary medicine2021
LINC01089 suppresses lung adenocarcinoma cell proliferation and migration via miR-301b-3p/STARD13 axis.
Article in BMC pulmonary medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- lncRNAs'p potential roles in the pathogenesis of cancer via interacting with signaling pathways; special focus on lncRNA-mediated signaling dysregulation in lung cancer.Medical oncology (Northwood, London, England) · 2024Review
- LINC01089 in cancer: multifunctional roles and therapeutic implications.Journal of translational medicine · 2024Review
- Loss of STARD13 contributes to aggressive phenotype transformation and poor prognosis in papillary thyroid carcinoma.Endocrine · 2024Article
- Differential expression and clinical significance of long non-coding RNAs in the development and progression of lung adenocarcinoma.Frontiers in oncology · 2024Review
- MicroRNA‑mediated regulation in lung adenocarcinoma: Signaling pathways and potential therapeutic implications (Review).Oncology reports · 2023Review
- Preparation, characterisation, and in vitro cancer-suppression function of RNA nanoparticles carrying miR-301b-3p Inhibitor.IET nanobiotechnology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung adenocarcinoma (LUAD) is one of the most common cancers with high morbidity and mortality worldwide. Long non-coding RNAs (lncRNAs) serve as tumor promoters or suppressors in the development of various human malignancies, including LUAD. Although long intergenic non-protein coding RNA 1089 (LINC01089) suppresses the progression of breast cancer, its mechanism in LUAD requires further exploration. Thus, we aimed to investigate the underlying function and mechanism of LINC01089 in LUAD.
methodsThe expression of LINC01089 in LUAD and normal cell lines was detected. Functional assays were applied to measure cell proliferation, apoptosis and migration. Besides, mechanism experiments were employed for assessing the interplay among LINC01089, miR-301b-3p and StAR related lipid transfer domain containing 13 (STARD13). Data achieved in this study was statistically analyzed with Student's t test or one-way analysis of variance.
resultsLINC01089 expression was significantly down-regulated in LUAD tissues and cells and its overexpression could reduce cell proliferation and migration. Moreover, LINC01089 could regulate STARD13 expression through competitively binding to miR-301b-3p in LUAD. Additionally, rescue assays uncovered that STARD13 depletion or miR-301b-3p overexpression could countervail the restraining effect of LINC01089 knockdown on the phenotypes of LUAD cells.
conclusionLINC01089 served as a tumor-inhibitor in LUAD by targeting miR-301b-3p/STARD13 axis, providing an innovative insight into LUAD therapies. Trial registration Not applicable.
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