Evidence map›Paper›PMID 35150399›Full record

ArticleGenes & genomics2022

Centromere protein N promotes lung adenocarcinoma progression by activating PI3K/AKT signaling pathway.

Yi Zheng, Hui You, Jingzhu Duan, Biyu Chen, Chenlin Wu, Peipei Chen, Meifang Wang

Abstract read
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In one paragraph

Article in Genes & genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

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  2. Balkan medical journal · 2026
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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

7 authors at 1 institution in 1 country.

Yi Zheng *Department of Respiratory and Critical Care Medicine, Taihe Hospital, Hubei University of Medicine, No. 32, Renmin South Road, Maojian District, Shiyan, 442000, Hubei, China.
Hui You *Department of Respiratory and Critical Care Medicine, Taihe Hospital, Hubei University of Medicine, No. 32, Renmin South Road, Maojian District, Shiyan, 442000, Hubei, China.
Jingzhu DuanDepartment of Respiratory and Critical Care Medicine, Taihe Hospital, Hubei University of Medicine, No. 32, Renmin South Road, Maojian District, Shiyan, 442000, Hubei, China.
Biyu ChenDepartment of Respiratory and Critical Care Medicine, Taihe Hospital, Hubei University of Medicine, No. 32, Renmin South Road, Maojian District, Shiyan, 442000, Hubei, China.
Chenlin WuDepartment of Respiratory and Critical Care Medicine, Taihe Hospital, Hubei University of Medicine, No. 32, Renmin South Road, Maojian District, Shiyan, 442000, Hubei, China.
Peipei ChenDepartment of Respiratory and Critical Care Medicine, Taihe Hospital, Hubei University of Medicine, No. 32, Renmin South Road, Maojian District, Shiyan, 442000, Hubei, China.
Meifang WangDepartment of Respiratory and Critical Care Medicine, Taihe Hospital, Hubei University of Medicine, No. 32, Renmin South Road, Maojian District, Shiyan, 442000, Hubei, China. wangmeifangwmf@163.com.ORCID 0000-0002-9380-4897
Hubei University of Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAs an important member of centromere family, centromere associated protein N (CENPN) was abnormally expressed in varied malignant tumors.

objectiveThis paper aimed to analyze the expression and related mechanism of CENPN in lung adenocarcinoma (LUAD).

methodsThe expression of CENPN in LUAD was analyzed by Gene Expression Profiling Interactive Analysis (GEPIA) database. The mRNA expression, protein expression, cell viability, cell invasion, cell apoptosis, cell stem like characteristics were detected by RT-PCR, western blot, CCK8 assay, transwell assay, flow cytometry and spheroidization assay, respectively. Finally, the pathological changes of xenograft were estimated by H&E staining, and the expression of proteins was detected by immunohistochemistry.

resultsGEPIA analysis showed that the CENPN expression in LUAD was significantly higher than that in normal lung tissue, which was negatively correlated with the prognosis. These results were consistent with our clinical data. Besides, CENPN was highly expressed in LUAD cell lines. In addition, the upregulation of CENPN amplified the cell viability, stemness and invasive ability in PC9 cells. However, the knockdown of CENPN inhibited the cell activity, stemness, invasive ability with increased cell apoptosis in A549. Furthermore, CENPN could positively regulate the phosphorylation of PI3K and AKT. The PI3K inhibitor, 740Y-P, could reverse the effect of CENPN silencing on the expression of Ki-67, cleaved caspase 3, OCT4, and snail 1. Finally, the downregulation of CENPN restrained the growth of xenograft and inactivated the PI3K/AKT pathway.

conclusionCENPN was abnormally overexpressed in LUAD, and promoted tumor progression of LUAD by affecting PI3K/AKT pathway.

Indexed as

Adenocarcinoma of LungLung NeoplasmsCell Line, TumorCell ProliferationCentromereChromosomal Proteins, Non-HistoneGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionCENPN protein, humanChromosomal Proteins, Non-HistonePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCENPNLung adenocarcinomaPI3K/AKT pathway

Identifiers

PMID35150399
OpenAlexW4211239375

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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.