Evidence map›Paper›PMID 30594196›Full record

ArticleRespiratory research2018

Investigating the mechanism by which SMAD3 induces PAX6 transcription to promote the development of non-small cell lung cancer.

Zhe Qian, Qiankun Zhang, Ying Hu, Tongmei Zhang, Jie Li, Zan Liu, Hua Zheng, Yuan Gao, Wenyun Jia, Aimin Hu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  17. International journal of molecular sciences · 2020
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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

12 authors at 2 institutions in 1 country.

Zhe QianDepartment of General Medicine, Beijing Chest Hospital, Capital Medical University & Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Yard, Beiguan Street, Tongzhou District, Beijing, 101149, China.
Qiankun ZhangDepartment of Medical Oncology, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Shushan District, Hefei, 230022, Anhui, China.
Ying HuDepartment of General Medicine, Beijing Chest Hospital, Capital Medical University & Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Yard, Beiguan Street, Tongzhou District, Beijing, 101149, China.
Tongmei ZhangDepartment of General Medicine, Beijing Chest Hospital, Capital Medical University & Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Yard, Beiguan Street, Tongzhou District, Beijing, 101149, China.
Jie LiDepartment of General Medicine, Beijing Chest Hospital, Capital Medical University & Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Yard, Beiguan Street, Tongzhou District, Beijing, 101149, China.
Zan LiuDepartment of General Medicine, Beijing Chest Hospital, Capital Medical University & Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Yard, Beiguan Street, Tongzhou District, Beijing, 101149, China.
Hua ZhengDepartment of General Medicine, Beijing Chest Hospital, Capital Medical University & Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Yard, Beiguan Street, Tongzhou District, Beijing, 101149, China.
Yuan GaoDepartment of General Medicine, Beijing Chest Hospital, Capital Medical University & Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Yard, Beiguan Street, Tongzhou District, Beijing, 101149, China.
Wenyun JiaDepartment of General Medicine, Beijing Chest Hospital, Capital Medical University & Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Yard, Beiguan Street, Tongzhou District, Beijing, 101149, China.
Aimin HuDepartment of General Medicine, Beijing Chest Hospital, Capital Medical University & Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Yard, Beiguan Street, Tongzhou District, Beijing, 101149, China.
Baolan LiDepartment of General Medicine, Beijing Chest Hospital, Capital Medical University & Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Yard, Beiguan Street, Tongzhou District, Beijing, 101149, China. libaolan1109@163.com.ORCID http://orcid.org/0000-0002-4953-0673
Jiqing HaoDepartment of Medical Oncology, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Shushan District, Hefei, 230022, Anhui, China. ayfy_hjq@163.com.
Capital Medical University · CNAnhui Medical University · CN

Funding

The Capital Health Research and Development of Special 2016-4-2161
6 · The paper itself

Abstract

backgroundThis study investigated the function of SMAD3 (SMAD family member 3) in regulating PAX6 (paired box 6) in non-small cell lung cancer.

methodsFirst, qRT-PCR was employed to detect SMAD3 expression in cancer tissues along with normal tissues and four cell lines, including BEAS-2B, H125, HCC827 and A549 cells. SMAD3 was knocked down by small interference RNA (siRNA), and then its expression was determined via qRT-PCR and Western blot analysis. The correlation between SMAD3 and PAX6 was determined by double luciferase reporter experiments and chromatin immunoprecipitation (ChIP) assay. Cell viability was evaluated by CCK-8 and colony forming assays, while cell migration and invasion were detected by Transwell analysis.

resultsSMAD3 and PAX6 were upregulated in lung cancer tissues and cancer cells. Knocking down SMAD3 and PAX6 by transfection with siRNAs specifically suppressed the expression of SMAD3 and PAX6 mRNA and protein levels. SMAD3 could promote PAX6 transcriptional activity by binding to its promoter. Reduced expression of SMAD3 led to the downregulation of PAX6 mRNA and protein levels along with decreased cell migration, invasion, proliferation and viability in A549 and HCC827 cells. PAX6 overexpression altered the si-SMAD3-induced inhibition of cell migration, invasion, proliferation and viability in A549 and HCC827 cells. Additionally, PAX6 knockdown alone also repressed the cell migration, invasion, proliferation and viability of the cell lines.

conclusionsSMAD3 promotes the progression of non-small cell lung cancer by upregulating PAX6 expression.

Indexed as

A549 CellsBiomarkers, TumorCarcinoma, Non-Small-Cell LungGene Expression Regulation, NeoplasticHumansLung NeoplasmsPAX6 Transcription FactorSmad3 ProteinTranscription, GeneticBiomarkers, TumorPAX6 protein, humanPAX6 Transcription FactorSmad3 ProteinSMAD3 protein, humanNon-small cell lung cancerPAX6SMAD3

Identifiers

PMID30594196
PMCPMC6311080
OpenAlexW2906880873

What OpenQuestion holds

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LicenceCC BY
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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.