Evidence map›Paper›PMID 34660326›Full record

ArticleFrontiers in oncology2021

Identification of CDCA2 as a Diagnostic and Prognostic Marker for Hepatocellular Carcinoma.

Zhenjun Yu, Yu Zhang, Shuai Shao, Qi Liu, Yuhan Li, Xiaoxiao Du, Kun Zhang, Mengxia Zhang, Haixia Yuan, Qiang Yuan and 5 more

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

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Overexpression ofInternational journal of molecular sciences · 2025
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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

15 authors at 3 institutions in 1 country.

Zhenjun YuDepartment of Hepatology and Gastroenterology, The Third Central Clinical College of Tianjin Medical University, Tianjin, China.
Yu ZhangDepartment of Hepatology and Gastroenterology, The Third Central Clinical College of Tianjin Medical University, Tianjin, China.
Shuai ShaoDepartment of Hepatology and Gastroenterology, Tianjin Union Medical Center Affiliated to Nankai University, Tianjin, China.
Qi LiuDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Yuhan LiDepartment of Hepatology and Gastroenterology, The Third Central Clinical College of Tianjin Medical University, Tianjin, China.
Xiaoxiao DuDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Kun ZhangDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Mengxia ZhangDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Haixia YuanDepartment of Hepatology and Gastroenterology, The Third Central Clinical College of Tianjin Medical University, Tianjin, China.
Qiang YuanDepartment of Hepatobiliary Surgery, The Tianjin Third Central Hospital, Tianjin, China.
Tong LiuTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, The Tianjin Third Central Hospital, Tianjin, China.
Yingtang GaoTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, The Tianjin Third Central Hospital, Tianjin, China.
Yijun WangDepartment of Hepatobiliary Surgery, The Tianjin Third Central Hospital, Tianjin, China.
Wei HongDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Tao HanDepartment of Hepatology and Gastroenterology, The Third Central Clinical College of Tianjin Medical University, Tianjin, China.
Tianjin Medical University · CNNankai University · CNTianjin Third Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveHepatocellular carcinoma (HCC) is one of the most common and malignant tumors with an insidious onset, difficult early diagnosis, and limited therapy options, resulting in a poor prognosis. Cell division cycle associated 2 (CDCA2), also known as Repo-Man, plays an important role in regulating mitosis and DNA repair, but the involvement of CDCA2 in HCC remains unclear.

methodsThe differentially expressed genes that were significantly upregulated in multiple RNA sequencing datasets of HCC were screened. Receiver operating characteristic (ROC) curve analysis was performed to identify diagnostic markers for HCC. Least absolute shrinkage and selection operator Cox regression analysis was performed to screen the prognosis-related genes. The screening and analyses identified CDCA2 as the target gene in this study. The expression of CDCA2 was analyzed in public databases and clinical specimens, and CDCA2 involvement in HCC was explored by both bioinformatic analysis and

resultsThe level of CDCA2 was enhanced in HCC compared with healthy livers. Overexpression of CDCA2 positively correlated with the pathological grade and TNM stage of the diseases. Furthermore, CDCA2 was found to be an independent prognostic predictor. An excellent prognostic model of HCC was successfully constructed with CDCA2 in combination with TNM stage. Bioinformatic analysis revealed that CDCA2 was closely associated with the cell cycle, apoptosis, and p53 signaling pathway. Silencing CDCA2 in Huh7 cells resulted in significant upregulation of p53 and the downstream PUMA and NOXA and a subsequently increased apoptosis. Inhibition of p53 signaling and apoptosis was found after overexpression of CDCA2 in L02 cells. Strikingly, the proliferation of cells was not affected by CDCA2.

conclusionsCDCA2 was a novel diagnostic marker for HCC, and overexpression of this gene reflected poor pathological grade, stage, and clinical prognosis. CDCA2 promoted the pathogenesis of HCC by suppressing the p53-PUMA/NOXA signaling and the subsequent apoptosis.

Indexed as

bioinformaticsbiomarkerCDCA2hepatocellular carcinomaprognosis

Identifiers

PMID34660326
PMCPMC8517522
OpenAlexW3204105165

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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.