Evidence map›Paper›PMID 36869643›Full record

ArticleThoracic cancer2023

Epigenetic and genetic inactivation of tumor suppressor miR-135a in non-small-cell lung cancer.

Jin Eun Choi, Hyo Sung Jeon, Hyun Jung Wee, Ji Yun Lee, Won Kee Lee, Shin Yup Lee, Seung Soo Yoo, Sun Ha Choi, Dong Sun Kim, Jae Yong Park

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Thoracic cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 25% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.

  1. Pooled it
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Jin Eun ChoiCell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu, South Korea.ORCID 0000-0001-7833-2257
Hyo Sung JeonCell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu, South Korea.
Hyun Jung WeeCell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu, South Korea.
Ji Yun LeeCell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu, South Korea.
Won Kee LeeBiostatistics, Medical Research Collaboration Center in Kyungpook National University Hospital and School of Medicine, Kyungpook National University, Daegu, South Korea.
Shin Yup LeeDepartment of Internal Medicine, School of Medicine, Kyungpook National University, Daegu, South Korea.ORCID 0000-0002-2121-7335
Seung Soo YooDepartment of Internal Medicine, School of Medicine, Kyungpook National University, Daegu, South Korea.ORCID 0000-0002-7309-9254
Sun Ha ChoiDepartment of Internal Medicine, School of Medicine, Kyungpook National University, Daegu, South Korea.
Dong Sun KimCell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu, South Korea.
Jae Yong ParkCell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu, South Korea.ORCID 0000-0001-7993-4495
Kyungpook National University · KRKyungpook National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDespite therapeutic advances, lung cancer prognosis remains poor. Loss of heterozygosity (LOH) in the 3p21 region is well documented in lung cancer, but the specific causative genes have not been identified. MATERIALS AND

methodsHere, we aimed to examine the clinical impact of miR-135a, located in the 3p21 region, in lung cancer. miR-135a expression was assessed using quantitative real-time polymerase chain reaction. LOH was analyzed at microsatellite loci D3S1076 and D3S1478, and promoter methylation status was determined by pyrosequencing of resected samples of primary non-small-cell lung cancer (NSCLC). The regulation of telomerase reverse transcriptase (TERT) was evaluated in lung cancer cells H1299 by luciferase report assays after treatment with miR-135a mimics.

resultsmiR-135a was significantly downregulated in squamous cell cancer (SCC) tumor tissues compared to normal tissues (p = 0.001). Low miR-135a expression was more frequent in patients with SCC (p = 2.9 × 10

conclusionThese results suggest that miR-135a may act as a tumor suppressor to play an important role in lung cancer carcinogenesis, which will provide a new insight into the translational value of miR-135a. Further large-scale studies are required to confirm these findings.

Indexed as

Carcinoma, Non-Small-Cell LungCarcinoma, Squamous CellLung NeoplasmsMicroRNAsGene Expression Regulation, NeoplasticGene SilencingGenes, Tumor SuppressorHumansMicroRNAsMIRN135 microRNA, humanDNA methylationloss of heterozygositymethylation prediction regionmiR-135anon-small-cell lung cancer

Identifiers

PMID36869643
PMCPMC10101835
OpenAlexW4323050310

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.