Evidence map›Paper›PMID 40031980›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2025

[High expression of apolipoprotein C1 promotes proliferation and inhibits apoptosis of papillary thyroid carcinoma cells by activating the JAK2/STAT3 signaling pathway].

Yu Bin, Ziwen Li, Suwei Zuo, Sinuo Sun, Min Li, Jiayin Song, Xu Lin, Gang Xue, Jingfang Wu

Abstract readEnglish Abstract
PubMed Full text at PMC Publisher
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Yu BinLaboratory of Morphology, Hebei North University, Zhangjiakou 075000, China.
Ziwen LiLaboratory of Morphology, Hebei North University, Zhangjiakou 075000, China.
Suwei ZuoLaboratory of Morphology, Hebei North University, Zhangjiakou 075000, China.
Sinuo SunLaboratory of Morphology, Hebei North University, Zhangjiakou 075000, China.
Min LiDepartment of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China.
Jiayin SongDepartment of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China.
Xu LinLaboratory of Morphology, Hebei North University, Zhangjiakou 075000, China.
Gang XueDepartment of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China.
Jingfang WuLaboratory of Morphology, Hebei North University, Zhangjiakou 075000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate the expression of apolipoprotein C1 (APOC1) in papillary thyroid carcinoma (PTC) and its effects on proliferation and apoptosis of PTC cells.

methodsThe expression level of APOC1 in PTC and its impact on prognosis were analyzed using GEPIA 2 and Kaplan-Meier databases. Immunohistochemistry (IHC) and Western blotting were used to detect the expression of APOC1 in PTC and adjacent tissues and in 3 PTC cell lines and normal thyroid Nthyori 3-1 cells. In TPC-1 and BCPAP cells, the effect of Lipofectamine 2000-mediated transfection with APOC1 siRNA or an APOC1-overexpressing plasmid on cell growth and colony formation ability were examined by observing the growth curves and using colony-forming assay. The changes in cell cycle and apoptosis of the transfected cells were analyzed with flow cytometry. RT-qPCR and Western blotting were used to detect the changes in expressions of P21, P27, CDK4, cyclin D1, Bcl-2, Bax, caspase-3 and caspase-9 and the key proteins in the JAK2/STAT3 signaling pathway.

resultsAPOC1 expression was significantly higher in PTC tissues and the 3 PTC cell lines than in the adjacent tissues and Nthyori 3-1 cells, respectively. In TPC-1 and BCPAP cells, APOC1 knockdown obviously reduced cell proliferative activity, increased the percentage of G0/G1 phase cells, lowered the percentages of S and G2 phase cells, promoted cell apoptosis, and downregulated mRNA and protein expression levels of CDK4, cyclin D1 and Bcl-2 and the protein levels of p-JAK2 and p-STAT3. APOC1 overexpression in the cells produced the opposite effects on cell proliferation, apoptosis, cell cycle and the mRNA and protein expressions. The application of AG490, a JAK2 inhibitor, strongly attenuated APOC1 overexpression-induced activation of the JAK2/STAT3 signaling pathway in BCPAP cells.

conclusionsAPOC1 overexpression promotes proliferation and inhibits apoptosis of PTC cells possibly by activating the JAK2/STAT3 signaling pathway and accelerating cell cycle progression.

Indexed as

ApoptosisJanus Kinase 2STAT3 Transcription FactorThyroid NeoplasmsCarcinoma, PapillaryCell Line, TumorCell ProliferationHumansSignal TransductionThyroid Cancer, PapillaryJAK2 protein, humanJanus Kinase 2STAT3 protein, humanSTAT3 Transcription Factorapolipoprotein C1apoptosisJAK2/STAT3 signaling pathwaypapillary thyroid carcinomaproliferation

Identifiers

PMID40031980
PMCPMC11875846

What OpenQuestion holds

Textmetadata
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.