Evidence map›Paper›PMID 30485570›Full record

ArticleCell proliferation2019

MiR-326/Sp1/KLF3: A novel regulatory axis in lung cancer progression.

Rong Wang, Jiali Xu, Jing Xu, Wei Zhu, Tianzhu Qiu, Jun Li, Meiling Zhang, Qianqian Wang, Tongpeng Xu, Renhua Guo and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 63 citations in OpenAlex.

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  17. Integration of TE Induces Cancer Specific Alternative Splicing Events.International journal of molecular sciences · 2022
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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

19 authors at 3 institutions in 1 country.

Rong WangDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Jiali XuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Jing XuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Wei ZhuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Tianzhu QiuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Jun LiDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Meiling ZhangDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Qianqian WangDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Tongpeng XuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Renhua GuoDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Kaihua LuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Yongmei YinDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Yanhong GuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Lingjun ZhuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Puwen HuangDepartment of Oncology, Liyang people's Hospital of Jiangsu Province, Liyang, China.
Ping LiuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Lianke LiuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Wei DeDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, China.
Yongqian ShuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.ORCID http://orcid.org/0000-0002-4684-2540
Jiangsu Province Hospital · CNDeyang Stomatological Hospital · CNNanjing Medical University · CN

Funding

Jiangsu ProvinceJiangsu Province Natural Science Foundation of China BK2015-1028National Natural Science Foundation of China 81502513National Natural Science Foundation of China BK2015-1028National Natural Science Foundation of China JX10231801Priority Academic Program Development of Jiangsu Higher Education Institutions JX10231801
6 · The paper itself

Abstract

objectivesTo investigate the function and regulatory mechanism of Krüppel-like factor 3 (KLF3) in lung cancer. MATERIALS AND

methodsKLF3 expression was analysed by qRT-PCR and Western blot assays. The proliferation, migration, invasion, cycle and apoptosis were measured by CCK-8 and EdU, wound-healing and Transwell, and flow cytometry assays. The tumour growth was detected by nude mouse tumorigenesis assay. In addition, the interaction between KLF3 and Sp1 was accessed by luciferase reporter, EMSA and ChIP assay. JAK2, STAT3, PI3K and p-AKT levels were evaluated by Western blot and IHC assays.

resultsThe results indicated that KLF3 expression was elevated in lung cancer tissues. Knockdown of KLF3 inhibited lung cancer cell proliferation, migration and invasion, and induced cell cycle arrest and apoptosis. In addition, the downregulation of KLF3 suppressed tumour growth in vivo. KLF3 was transcriptionally activated by Sp1. miR-326 could bind to 3'UTR of Sp1 but not KLF3 and decreased the accumulation of Sp1, which further indirectly reduced KLF3 expression and inactivated JAK2/STAT3 and PI3K/AKT signaling pathways in vitro and in vivo.

conclusionsOur data demonstrate that miR-326/Sp1/KLF3 regulatory axis is involved in the development of lung cancer, which hints the potential target for the further therapeutic strategy against lung cancer.

Indexed as

Gene Expression Regulation, NeoplasticA549 CellsAgedAnimalsApoptosisCell MovementCell ProliferationDisease ProgressionFemaleHumansKruppel-Like Transcription FactorsLung NeoplasmsMaleMice, NudeMicroRNAsMiddle AgedKLF3 protein, humanKruppel-Like Transcription FactorsMicroRNAsMIRN326 microRNA, humanSp1 Transcription FactorKLF3lung cancermicroRNA-326SP1

Identifiers

PMID30485570
PMCPMC6495967
OpenAlexW2903074732

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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.