Evidence map›Paper›PMID 32960462›Full record

ArticleJournal of clinical laboratory analysis2021

CKS1B promotes cell proliferation and invasion by activating STAT3/PD-L1 and phosphorylation of Akt signaling in papillary thyroid carcinoma.

Hui Wang, Zhengdong Zhang, Zhe Yan, Shihong Ma

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

12 citing papers in PubMed, 18 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

4 authors at 1 institution in 1 country.

Hui WangShanghai Xuhui Center Hospital, Shanghai, China.
Zhengdong ZhangShanghai Xuhui Center Hospital, Shanghai, China.
Zhe YanShanghai Xuhui Center Hospital, Shanghai, China.
Shihong MaShanghai Xuhui Center Hospital, Shanghai, China.ORCID https://orcid.org/0000-0002-5548-9777
Shanghai Xuhui Central Hospital · CN

Funding

Clinical Medicine Science and Technology Development Fund of Jiangsu University JLY20180041Xuhui District Central Hospital Project 2018XHYY-10
6 · The paper itself

Abstract

objectiveTo investigate role of GKS1B and its relationship between STAT3/PD-L1 and p-Akt in papillary thyroid carcinoma (PTC).

methodsExpression of GKS1B and PD-L1 was determined in PTC cell lines. GKS1B was overexpressed or knocked down by transfection with overexpression plasmids or si-CKS1B. STAT3 inhibitor WP1066 was used to suppress STAT3, and PD-L1 inhibitor Pembrolizumab was used to block PD-L1. Cell viability and invasion were evaluated by MTT and transwell assay, respectively. The expression of STAT3, p-STAT3, Akt, and p-Akt was measured using Western blotting.

resultsBoth protein levels and mRNA levels of CKS1B and PD-L1 were remarkably up-regulated in PTC cell lines. Knockdown of CKS1B significantly inhibited cell viability and invasion of PTC cells and suppressed STAT3/PD-L1 signaling and Akt phosphorylation, while overexpression of CKS1B led to opposite results. Inhibition of STAT3 or PD-L1 reversed the effects of overexpressed CKS1B on PTC cells.

conclusionThe overexpression of CSK1B could promote cell viability and invasion of PTC cells through activation of STAT3/PD-L1 signaling and Akt phosphorylation.

Indexed as

B7-H1 AntigenCDC2-CDC28 KinasesSTAT3 Transcription FactorThyroid Cancer, PapillaryThyroid NeoplasmsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessPhosphorylationSignal TransductionB7-H1 AntigenCD274 protein, humanCDC2-CDC28 KinasesCKS1B protein, humanSTAT3 protein, humanSTAT3 Transcription FactorAktCKS1Bpapillary thyroid carcinomaSTAT3/PD-L1

Identifiers

PMID32960462
PMCPMC7843292
OpenAlexW3087433574

What OpenQuestion holds

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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.