Evidence map›Paper›PMID 34281492›Full record

ArticleBioengineered2021

Transcription factor specificity protein 1-mediated Serine/threonine kinase 39 upregulation promotes the proliferation, migration, invasion and epithelial-mesenchymal transition of hepatocellular carcinoma cells by activating the transforming growth factor-β1 /Smad2/3 pathway.

Jing Wang, Zhenyu Fan, Jia Li, Jingmao Yang, Xiaofei Liu, Jilin Cheng

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bioengineered, 2021. 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 18% 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, 14 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

6 authors at 4 institutions in 1 country.

Jing WangDepartment of Hepatology, Tianjin Institute of Hepatology, Tianjin Second People's Hospital, Tianjin, China.
Zhenyu FanDepartment of Gastroenterology and Hepatology, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Jia LiDepartment of Hepatology, Tianjin Institute of Hepatology, Tianjin Second People's Hospital, Tianjin, China.
Jingmao YangDepartment of Gastroenterology and Hepatology, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Xiaofei LiuDepartment of Gastroenterology and Hepatology, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Jilin ChengDepartment of Gastroenterology and Hepatology, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Fudan University · CNShanghai Public Health Clinical Center · CNTianjin People's Hospital · CNXian Yang Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bioinformatics analysis showed that Serine/threonine kinase 39 (STK39), which was testified to play an important role in human cancers, may be a hub gene in diagnosing hepatocellular carcinoma (HCC). This study aimed to explore whether STK39 could be regulated by specificity protein 1 (SP1) to affect HCC cells malignant processes. Firstly, STK39 expression in tissues of HCC patients and several cell lines was analyzed. After STK39 silencing, cell proliferation was evaluated by methyl thiazolyl tetrazolium and colony formation assay. Tunel staining was used to detect cell apoptosis. Then, the abilities of cell migration and invasion were determined with wound healing and transwell assays. The expression of epithelial-mesenchymal transition (EMT)-related proteins and transforming growth factor-β1 (TGF-β1)/Smad2/3 pathway proteins was tested by western blot analysis. Thereafter, cells were overexpressed with SP1 under the circumstance of STK39 knockdown, and then the above cellular processes were under observation. Results revealed that the increased expression of STK39, which was found in both HHC patients and HCC cell lines, exhibited poor HCC prognosis. STK39 silencing inhibited Hep3b cell proliferation, migration, invasion, EMT and TGF-β1/Smad2/3 expression but promoted cell apoptosis. Additionally, SP1 could bind to the STK39 promoter and facilitate STK39 expression. Further studies revealed that the effects of STK39 silencing on Hep3b cells were blocked by SP1 overexpression. In conclusion, SP1-mediated STK39 up-regulation leads to the increased proliferation, migration, invasion and EMT of HCC cells via activating TGF-β1/Smad2/3 pathway. Therapies that target SP1 to knockdown STK39 expression may contribute to the inhibition of HCC progression.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell Line, TumorCell MovementCell ProliferationDatabases, GeneticEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansProtein Serine-Threonine KinasesSignal TransductionSmad2 ProteinSmad3 ProteinSp1 Transcription FactorTransforming Growth Factor beta1Protein Serine-Threonine KinasesSmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanSP1 protein, humanSp1 Transcription FactorSTK39 protein, humanTGFB1 protein, humanTransforming Growth Factor beta1Hepatocellular carcinomaSerine/threonine kinase 39Smad2/3specificity protein 1transforming growth factor β1

Identifiers

PMID34281492
PMCPMC8806741
OpenAlexW3185960729

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.