Evidence map›Paper›PMID 29618932›Full record

ArticleOncoTargets and therapy2018

miR-1269 promotes cell survival and proliferation by targeting tp53 and caspase-9 in lung cancer.

Min Bao, Yingjian Song, Jingjing Xia, Pengling Li, Qing Liu, Zongren Wan

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Bioinformatics analysis of BIRC5 in human cancers.Annals of translational medicine · 2022
    Article
  2. Article
  3. miR-1269a and miR-1269b: Emerging Carcinogenic Genes of the miR-1269 Family.Frontiers in cell and developmental biology · 2022
    Review
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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

6 authors at 1 institution in 1 country.

Min BaoDepartment of Pneumology, Huai'an First People's Hospital, Huai'an, China.
Yingjian SongDepartment of Pneumology, Huai'an First People's Hospital, Huai'an, China.
Jingjing XiaDepartment of Pneumology, Huai'an First People's Hospital, Huai'an, China.
Pengling LiDepartment of Pneumology, Huai'an First People's Hospital, Huai'an, China.
Qing LiuDepartment of Pneumology, Huai'an First People's Hospital, Huai'an, China.
Zongren WanDepartment of Pneumology, Huai'an First People's Hospital, Huai'an, China.
Huaian First People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimLung cancer is the leading cause of cancer death worldwide. In this study, we aim to elucidate the role of miR-1269 in the pathogenesis of lung cancer. METHODS AND

resultsFrom the results of analyses using The Cancer Genome Atlas (TCGA) database, we noted the expression of miR-1269 was increased in lung cancer tissue. miR-1269 expression was detected in both the normal adjacent lung tissue and in the tumorous lung tissue of lung cancer patients, and miR-1269 was more highly expressed in the tumors. High expression of miR-1269 correlated with patients' tumor stage and lymph node metastasis. A Cell Counting Kit-8 (CCK8) analysis and a cloning formation assay showed that overexpression of miR-1269 significantly promoted the growth of A549 cells, and that a lower expression of miR-1269 significantly increased cell apoptosis. We used the TargetScan 6.2 Database to predict the potential targets of miR-1269, and a luciferase activity assay was used to determine the direct interaction between miR-1269, tumor protein p53 (TP53), and caspase-9. Results from Western blots and real-time PCR showed that overexpression of miR-1269 significantly inhibited TP53 and caspase-9 expression. In addition, caspase-3 activity was found to decrease in a miR-1269 mimic group. The results showed that gene silencing of TP53 and caspase-9 significantly inhibited A549 cell growth and promoted cell apoptosis. The results also showed that the inhibition of miR-1269 and caspase-9 expression inhibited cell apoptosis. Immunohistochemistry (IHC) results demonstrated that TP53 and caspase-9 were expressed in low levels in tumor tissues, and that an inverse correlation exists between miR-1269 expression levels and TP53 or caspase-9 expression levels.

conclusionThese results demonstrate that miR-1269 promotes cell survival and proliferation by targeting TP53 and caspase-9 in lung cancer.

Indexed as

caspasecell apoptosislung carcinomamicroRNA-1269tumor protein p53

Identifiers

PMID29618932
PMCPMC5875400
OpenAlexW2790902657

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.