ArticleAmerican journal of translational research2021
Long non-coding RNA H19 and the underlying epigenetic function in response to DNA damage of lung cancer cells.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed.
- Divergent regulation of long non-coding RNAs H19 and PURPL affects cell senescence in human dermal fibroblasts.GeroScience · 2025Article
- A prominent role of LncRNA H19 in H. pylori CagA induced DNA damage response and cell malignancy.Scientific reports · 2024Article
- The role of long noncoding RNA H19 in gynecological pathologies: Insights into gene regulation and immune modulation (Review).International journal of molecular medicine · 2023Review
- Instrumental variable-based high-dimensional mediation analysis with unmeasured confounders for survival data in the observational epigenetic study.Frontiers in genetics · 2023Article
- Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of the current study is to clarify the epigenetic function of long non-coding RNA (lncRNA) H19 in lung cancer as well as the relevant regulatory mechanism. We first determined H19 upregulation in A549 cells. DNA damage model was established in A549 cells by exposure to X-ray and then ionizing radiation (IR). The degree of DNA damage in the IR cell model was assessed by Comet assay. Gain- and loss-of-function assays were employed to clarify the roles of H19 and miR-675 in DNA damage of A549 cells. The results demonstrated that H19 knockdown inhibited the response of lung cancer cells to IR-induced DNA damage but promoted the damage repair. H19 could interact with miR-675, whereby aggravating IR-induced DNA damage. Furthermore, p62 was identified to be a downstream gene positively regulated by miR-675 while APEX1 was a target gene negatively regulated by miR-625-5p. Meanwhile, silencing of H19 could inhibit APEX1 expression by upregulating miR-625-5p, thereby accelerating DNA damage repair in A549 cells. In conclusion, H19 could function as a modulator of DNA damage response in lung cancer cells.
Indexed as
Identifiers
34306329PMC8290785What OpenQuestion holds
Registered trials
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