Evidence map›Paper›PMID 29928883›Full record

ArticleBiochemical and biophysical research communications2018

Suppression of cleavage factor Im 25 promotes the proliferation of lung cancer cells through alternative polyadenylation.

Jingjing Huang, Tingting Weng, Junsuk Ko, Ning-Yuan Chen, Yu Xiang, Kelly Volcik, Leng Han, Michael R Blackburn, Xiang Lu

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

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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

24 citing papers in PubMed, 35 citations in OpenAlex.

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  9. 3'UTR shortening of HAS2 promotes hyaluronan hyper-synthesis and bioenergetic dysfunction in pulmonary hypertension.Matrix biology : journal of the International Society for Matrix Biology · 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

9 authors at 3 institutions in 2 countries.

Jingjing HuangDepartment of Geriatrics, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
Tingting WengDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center, Houston, TX, USA.
Junsuk KoDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center, Houston, TX, USA.
Ning-Yuan ChenDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center, Houston, TX, USA.
Yu XiangDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center, Houston, TX, USA.
Kelly VolcikDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center, Houston, TX, USA.
Leng HanDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center, Houston, TX, USA.
Michael R BlackburnDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center, Houston, TX, USA.
Xiang LuNanjing Medical University, Nanjing, Jiangsu, China. Electronic address: luxiang66@njmu.edu.cn.
The University of Texas Health Science Center at Houston · USNanjing Medical University · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

Adenosine Signaling and Lung FibrosisR01HL070952 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BLACKBURN, MICHAEL R · 2002 to 2019
$5.7M
NHLBI NIH HHS R01 HL070952
6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC) is a life-threatening disease that has a poor prognosis and low survival rate. Cleavage factor Im 25 (CFIm25) is a RNA-binding protein that if down-regulated causes 3'UTR shortening and thus promotes the transcript stability of target genes. It is not clear whether CFIm25 and alternative polyadenylation (APA) play a role during cancer development. The purpose of this study is to explore the role of CFIm25 in lung cancer cell proliferation.

methodsCFIm25 was knocked down in A549 cells. Western blots were carried out to determine the protein expression of CFIm25, insulin growth factor 1 receptor (IGF1R), CyclinD1 (CCND1) and TP53. Real-time qRT PCR was performed to determine the total transcript levels of CFIm25 targets and the normalized fold changes in their distal PAS (dPAS) usage. Immunofluorescence was carried out to check the expression of CFIm25, IGF1R and CCND1. Cell proliferation over time was determined using the WST-1 reagent.

resultsThe transcript levels of CCND1 and GSK3β were significantly increased and the dPAS usage of several oncogenes (IGF1R, CCND1 and GSK3β) were decreased after CFIm25 knockdown. The protein level of IGF1R was increased, and we detected increased percentage of CCND1 positive cells and cell proliferation over time in CFIm25 knockdown cells. In addition, the mRNA and APA analysis of IGF1R using patient RNA-seq data from the Cancer Genome Atlas indicated that IGF1R is shortened in both lung adenocarcinoma and lung squamous cell carcinoma compared to normal controls.

conclusionsOur findings suggest that CFIm25 plays an important role in lung cancer cell proliferation through regulating the APA of oncogenes, including IGF1R, and promoting their protein expression.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsA549 CellsAlternative SplicingCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellCell ProliferationCleavage And Polyadenylation Specificity FactorHumansLung NeoplasmsModels, GeneticmRNA Cleavage and Polyadenylation FactorsPolyadenylationReceptor, IGF Type 1Receptors, SomatomedinRNA Interference3' Untranslated RegionsCleavage And Polyadenylation Specificity FactorIGF1R protein, humanmRNA Cleavage and Polyadenylation FactorsNudt21 protein, humanReceptor, IGF Type 1Receptors, SomatomedinA549Alternative polyadenylationApoptosisCancerCyclinD1GSK3βIGF1RP53Proliferation

Identifiers

PMID29928883
PMCPMC6095800
OpenAlexW2810032171

What OpenQuestion holds

Textmetadata
LicenceTDM
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.