ArticleInternational journal of clinical and experimental pathology2017
Upregulated lncRNA H19 promotes non-small cell lung cancer cell proliferation through miR-138/PDK1 axis.
Article in International journal of clinical and experimental pathology, 2017. 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
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
7 citing papers in PubMed, 13 citations in OpenAlex.
- Role of long non-coding RNAs in the pathogenesis of gastric cancer-induced by Helicobacter pylori.Inflammopharmacology · 2025Review
- Long noncoding RNA (lncRNA)Genes & diseases · 2023Review
- Hsa_circ_0000418 promotes the progression of glioma by regulating microRNA-409-3p / pyruvate dehydrogenase kinase 1 axis.Bioengineered · 2022Article
- Long Noncoding RNAs in Lung Cancer: From Disease Markers to Treatment Roles.Cancer management and research · 2022Review
- LncRNA H19: A novel oncogene in multiple cancers.International journal of biological sciences · 2021Review
- LncRNAs in Non-Small-Cell Lung Cancer.Non-coding RNA · 2020Review
- Exosomal Long Non-Coding RNAs in Lung Diseases.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNA (lncRNA) H19 was reported to be aberrantly expressed and implicated in non-small cell lung cancer (NSCLC). However, the regulation of NSCLC progression by H19 was not well understood. In this study, we found that the expression level of H19 was obviously increased, but miR-138 was decreased in NSCLC tissues and NSCLC cells including A549, H1299 and H460 cells. Upregulation of H19 promotes cell proliferation ability in A549 and H460 cells, while downregulation of H19 did the opposite. H19 represses miR138 expression and H19 expression level was negatively correlated with miR-138 expression level in NSCLC tissues. Moreover, overexpression of mutant H19 (Mut-H19) has no effect on miR-138 expression in A549 and H460 cells. Dual luciferase reporter assay showed that PDK1 was a target gene of miR-138. Overexpression of H19 attenuated the inhibitory effect of miR-138 on PDK1 protein expression. The inhibition of NSCLC cell proliferation induced by H19 knockdown required the activity of miR-138, and could be reversed by overexpression of PDK1. Overall, we concluded that H19 upregulates the expression of PDK1 through downregulation of miR-138 to promote NSCLC cell proliferation. H19 could potentially be employed as a therapeutic target for the treatment of NSCLC.
Indexed as
Identifiers
31966771PMC6965484W3026450659What OpenQuestion 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 OpenQuestion graph.