Evidence map›Paper›PMID 36639822›Full record

ArticleExperimental hematology & oncology2023

CDCA8 induced by NF-YA promotes hepatocellular carcinoma progression by regulating the MEK/ERK pathway.

Erbao Chen, Yu He, Jing Jiang, Jing Yi, Zhilin Zou, Qiuzi Song, Qingqi Ren, Zewei Lin, Yi Lu, Jikui Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Experimental hematology & oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

23 citing papers in PubMed, 35 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

11 authors at 3 institutions in 1 country.

Erbao Chen *Department of Hepatobiliary and Pancreatic Surgery, Peking University Shenzhen Hospital, Shenzhen, 518036, Guangdong, China.
Yu He *School of Medicine, Southern University of Science and Technology, Shenzhen, 518055, Guangdong, China.
Jing Jiang *Department of Pathology, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Jing YiDepartment of Hepatobiliary and Pancreatic Surgery, Peking University Shenzhen Hospital, Shenzhen, 518036, Guangdong, China.
Zhilin ZouDepartment of Ophthalmology, Affiliated Eye Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Qiuzi SongDepartment of Hepatobiliary and Pancreatic Surgery, Peking University Shenzhen Hospital, Shenzhen, 518036, Guangdong, China.
Qingqi RenDepartment of Hepatobiliary and Pancreatic Surgery, Peking University Shenzhen Hospital, Shenzhen, 518036, Guangdong, China.
Zewei LinDepartment of Hepatobiliary and Pancreatic Surgery, Peking University Shenzhen Hospital, Shenzhen, 518036, Guangdong, China.
Yi LuSchool of Medicine, Southern University of Science and Technology, Shenzhen, 518055, Guangdong, China. luy3@sustech.edu.cn.
Jikui LiuDepartment of Hepatobiliary and Pancreatic Surgery, Peking University Shenzhen Hospital, Shenzhen, 518036, Guangdong, China. liu8929@126.com.
Jian ZhangSchool of Medicine, Southern University of Science and Technology, Shenzhen, 518055, Guangdong, China. zhangjian@sustech.edu.cn.
Peking University Shenzhen Hospital · CNSouthern University of Science and Technology · CNAffiliated Eye Hospital of Wenzhou Medical College · CN

Funding

China Postdoctoral Science Foundation 2020M682779National Natural Science Foundation of China 81972420National Natural Science Foundation of China 81972766Science, Technology and Innovation Commission of Shenzhen Municipality JCYJ20170412154619484Science, Technology and Innovation Commission of Shenzhen Municipality JCYJ20190809095801653Science, Technology and Innovation Commission of Shenzhen Municipality JCYJ20190809100217290Science, Technology and Innovation Commission of Shenzhen Municipality JCYJ20190809161811237
6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is one of the most lethal malignant tumors. Cell division cycle associated 8 (CDCA8) is an important multifactorial regulator in cancers. However, its up and downstream targets and effects in HCC are still unclear.

methodsA comprehensive bioinformatics analysis was performed using The Cancer Genome Atlas dataset (TCGA) to explore novel core oncogenes. We quantified CDCA8 levels in HCC tumors using qRT-PCR. HCC cell's proliferative, migratory, and invasive abilities were detected using a Cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2'-deoxyuridine (EdU) assay, clone formation, and a Transwell assay. An orthotopic tumor model and tail vein model were constructed to determine the effects of CDCA8 inhibition in vivo. The mechanism underlying CDCA8 was investigated using RNA sequencing. The prognostic value of CDCA8 was assessed with immunohistochemical staining of the tissue microarrays.

resultsCDCA8 was identified as a novel oncogene during HCC development. The high expression of CDCA8 was an independent predictor for worse HCC outcomes both in publicly available datasets and in our cohort. We found that CDCA8 knockdown inhibited HCC cell proliferation, colony formation, and migration by suppressing the MEK/ERK pathway in vitro. Moreover, CDCA8 deficiency significantly inhibited tumorigenesis and metastasis. Next-generation sequencing and laboratory validation showed that CDCA8 silencing inhibited the expression of TPM3, NECAP2, and USP13. Furthermore, NA-YA overexpression upregulated the expression of CDCA8. CDCA8 knockdown could attenuate NF-YA-mediated cell invasion in vitro. The expression of NF-YA alone or in combined with CDCA8 were validated as significant independent risk factors for patient survival.

conclusionOur findings revealed that the expression of CDCA8 alone or in combined with NF-YA contributed to cancer progression, and could serve as novel potential therapeutic targets for HCC patients.

Indexed as

Cancer metastasisCell division cycle associated 8Hepatocellular carcinomaNF-YAPrognosis

Identifiers

PMID36639822
PMCPMC9838039
OpenAlexW4316039521

What OpenQuestion holds

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LicenceCC BY
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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.