Evidence map›Paper›PMID 25404268›Full record

ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2014

[Mechanism of thymosin beta 10 inhibiting the apoptosis 
and prompting proliferation in A549 cells].

Zixuan Li, Lianyue Qu, Hongshan Zhong, Ke Xu, Xueshan Qiu

Open access · greenAbstract readEnglish Abstract
PubMed Full text at PMC Publisher
In one paragraph

Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed, 4 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Zixuan LiDepartment of Radiology and Key Laboratory of Diagnostic Imagingand Interventional Radiology, the First Affiliated Hospital of China Medical University, Shenyang 110001, China;Department of Pathology, the First Affiliated Hospital of China Medical University and College of Basic Medical Sciences, China Medical University, Shenyang 110001, China.
Lianyue QuDepartment of Pharmacy, the First Affiliated Hospital of China Medical University, Shenyang 110001, China.
Hongshan ZhongDepartment of Radiology and Key Laboratory of Diagnostic Imagingand Interventional Radiology, the First Affiliated Hospital of China Medical University, Shenyang 110001, China.
Ke XuDepartment of Radiology and Key Laboratory of Diagnostic Imagingand Interventional Radiology, the First Affiliated Hospital of China Medical University, Shenyang 110001, China.
Xueshan QiuDepartment of Pathology, the First Affiliated Hospital of China Medical University and College of Basic Medical Sciences, China Medical University, Shenyang 110001, China.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectiveThymosin beta 10 (Tβ10) is one of β-thymosin family members, has a highly conserved polar 5 kDa peptides. This peptide is now regarded to be a small actin-binding protein and thereby induce depolymerization of the intracellular F-actin networks. Alteration of Tβ10 expression may alter the balance of cell growth, cell death, cell attachment and cell migration. Tβ10 also affects cell metastasis as well as proliferation, apoptosis and vascularization of cancer cells. But function of Tβ10 appear to be rather different between cancer cells, and the molecular mechanisms of β-thymosins to regulate cell apoptosis and proliferation in NSCLC (non-small cell lung cancer) cell lines are unclear. In this study, we used lung adenocarcinoma cell line A549, added Tβ10 or down-regulated the expression of Tβ10. We observed the change of apoptosis, proliferation and cell cyclin ability in A549 and the mechanisms underline them were also identified.

methodsAfter A549 was treated with 100 ng/mL recombinant human Tβ10 or siTβ10, apoptosis rate of A549 and cell cycle distribution were detected by flow cytometry (FCM). CCK-8 assay was employed to determine the proliferation of A549. The mRNA level of P53, Caspase-3, Cyclin A and Cyclin E were determined by real-time PCR. The protein level of P53, Caspase-3, Cyclin A and Cyclin E were detected by Western blot.

resultsAdd Tβ10 can inhibit the apoptosis and prompt the proliferation of A549. It can also increase the cell rates of S-phrase and G2/M-phrase, decrease the expression of P53 and Caspase-3, but increase the expression of Cyclin A and Cyclin E. Interferance of Tβ10 can prompt the apoptosis and inhibit the proliferation of A549. It can also increase the cell rates of G0/G1-phrase, increase the expression of P53 and Caspase-3, but decrease the expression of Cyclin A and Cyclin E.

conclusionsIn lung cancer cell line, Tβ10 can inhibit the apoptosis by increase P53, drive cells into the S and G2/M-phase, prompt cell proliferation by increase the expression of Cyclin A and Cyclin E. Tβ10 may become a potential biomarker and therapy target for non-small cell lung cancer.

Indexed as

AdenocarcinomaApoptosisBlotting, WesternCaspase 3Cell CycleCell Line, TumorCell ProliferationCyclin ACyclin EFlow CytometryGene Expression Regulation, NeoplasticHumansLung NeoplasmsReverse Transcriptase Polymerase Chain ReactionRNA InterferenceThymosinCaspase 3Cyclin ACyclin EThymosinthymosin beta(10)Tumor Suppressor Protein p53

Identifiers

PMID25404268
PMCPMC6000358
OpenAlexW2197078998

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.