ArticleHeliyon2023
Association of long noncoding RNA MALAT1 with the radiosensitivity of lung adenocarcinoma cells via the miR-140/PD-L1 axis.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 9 citations in OpenAlex.
- Quercetin Affects Carcinogenic Phenotype of Breast and Lung Cancer Cells Differentially Through Sterol Regulation Mediated by MALAT1 Perturbation.Chemistry, an Asian journal · 2026Article
- Current insights into long non-coding RNAs role for insulin resistance emerging in type 2 diabetes mellitus and its complications.Toxicology reports · 2026Review
- LncRNAs: key regulators and molecular mechanisms in lung cancer radiosensitivity.Open medicine (Warsaw, Poland) · 2026Review
- Role of non-coding RNAs in radiotherapy sensitivity in non-small cell lung cancer.Discover oncology · 2025Review
- MALAT1 as a molecular driver of tumor progression, immune evasion, and resistance to therapy.Molecular cancer · 2025Review
- Roles of the phagocytosis checkpoint in radiotherapy.Cell death & disease · 2025Review
- Hsa_circ_0001492 regulates the hsa-miR-145-5p/ovarian carcinoma immunoreactive antigen domain 2 axis to promote the progression of lung adenocarcinoma.Biomolecules & biomedicine · 2025Article
- Comprehensive insights and In silico analysis into the emerging role of LincRNAs in lung diseases pathogenesis; a step toward ncRNA precision.Functional & integrative genomics · 2025Review
- Non-coding RNAs as potential mediators of resistance to lung cancer immunotherapy and chemotherapy.Oncology research · 2025Review
- Radiotherapy effects on the ceRNA network in high-risk prostate cancer patients.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2025Article
- Establishment of potential lncRNA-related hub genes involved competitive endogenous RNA in lung adenocarcinoma.BMC cancer · 2024Article
- MicroRNAs as regulators of immune checkpoints in cancer immunotherapy: targeting PD-1/PD-L1 and CTLA-4 pathways.Cancer cell international · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To investigate the effect of MALAT1 on the modulating the radiosensitivity of lung adenocarcinoma, through regulation of the expression of the miR-140/PD-L1 axis. Methods: The online databases UALCAN and dbDEMC were searched for the MALAT1 and miR-140 expressions in patients with lung adenocarcinoma (LUAD), respectively. Then analyze their relationship with overall survival rates separately in the UALCAN and ONCOMIR databases. A functional analysis was performed for A549 cells by transfecting small-interfering RNAs or corresponding plasmids after radiotherapy. Xenograft models of LUAD exposed to radiation were established to further observe the effects of MALAT1 on the radiosensitivity of LUAD. The luciferase assay and reverse transcription-polymerase chain reaction were performed to assess the interaction between miR-140 and MALAT1 or PD-L1. Results: MALAT1 were overexpressed in human LUAD tumor tissues and cell lines, while miR-140 were inhibited. MALAT1 knockdown or miR-140 increase suppressed cell proliferation and promoted cell apoptosis in LUAD after irradiation. LUAD xenograft tumor growth was also inhibited by MALAT1 knockdown combined with irradiation. miR-140 could directly bind with MALAT1 or PD-L1. Furthermore, MALAT1 knockdown inhibited PD-L1 mRNA and protein expressions by upregulating miR-140 in LUAD cells. Conclusion: MALAT1 may function as a sponge for miR-140a-3p to enhance the PD-L1 expression and decrease the radiosensitivity of LUAD. Our results suggest that MALAT1 might be a promising therapeutic target for the radiotherapy sensitization of LUAD.
Indexed as
Identifiers
What 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.