Evidence map›Paper›PMID 36056599›Full record

ArticleCancer science2023

CDCA7 promotes TGF-β-induced epithelial-mesenchymal transition via transcriptionally regulating Smad4/Smad7 in ESCC.

Hongyi Li, Shaojie Wang, Xiubo Li, Yongjia Weng, Dinghe Guo, Pengzhou Kong, Caixia Cheng, Yanqiang Wang, Ling Zhang, Xiaolong Cheng and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

13 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

11 authors at 1 institution in 1 country.

Hongyi LiDepartment of Pathology, School of Basic Medical Science, Shanxi Medical University, Taiyuan, China.
Shaojie WangDepartment of Pathology, School of Basic Medical Science, Shanxi Medical University, Taiyuan, China.
Xiubo LiDepartment of Pathology, School of Basic Medical Science, Shanxi Medical University, Taiyuan, China.
Yongjia WengDepartment of Pathology, School of Basic Medical Science, Shanxi Medical University, Taiyuan, China.
Dinghe GuoDepartment of Pathology, School of Basic Medical Science, Shanxi Medical University, Taiyuan, China.
Pengzhou KongDepartment of Pathology, School of Basic Medical Science, Shanxi Medical University, Taiyuan, China.
Caixia ChengDepartment of Pathology, The First Hospital, Shanxi Medical University, Taiyuan, China.
Yanqiang WangDepartment of Pathology, School of Basic Medical Science, Shanxi Medical University, Taiyuan, China.
Ling ZhangDepartment of Pathology, School of Basic Medical Science, Shanxi Medical University, Taiyuan, China.
Xiaolong ChengDepartment of Pathology, School of Basic Medical Science, Shanxi Medical University, Taiyuan, China.ORCID https://orcid.org/0000-0001-8726-5631
Yongping CuiDepartment of Pathology, School of Basic Medical Science, Shanxi Medical University, Taiyuan, China.
Shanxi Medical University · CN

Funding

Foundation for Youths of Shanxi Province 201901D211349National Natural Science Foundation of China 81602175National Natural Science Foundation of China U21A20372The National Key R&D Program of China 2021YFC2501001
6 · The paper itself

Abstract

Cell division cycle associated 7 (CDCA7) is a copy number amplification gene that contributes to the metastasis and invasion of tumors, including esophageal squamous cell carcinoma (ESCC). This present study aimed at clarifying whether high expression of CDCA7 promotes the metastasis and invasion of ESCC cell lines and exploring the underlying mechanisms implicated in epithelial-mesenchymal transition (EMT) of ESCC. The role of CDCA7 in the regulation of ESCC metastasis and invasion was evaluated using ESCC cell lines. Expression of EMT-related markers including E-cadherin, N-cadherin, Vimentin, Snail, and Slug, transforming growth factor β (TGF-β) signaling pathway including Smad2/3, p-Smad2/3, Smad4, and Smad7 were detected in CDCA7 knockdown and overexpressed cell lines. Dual-luciferase reporter assay and rescue assay were used to explore the underlying mechanisms that CDCA7 contributed to the metastasis and invasion of ESCC. High CDCA7 expression significantly promoted the metastasis and invasion of ESCC cell lines both in vivo and in vitro. Additionally, the expression of CDCA7 positively correlated with the expression of N-cadherin, Vimentin, Snail, Slug, TGF-β signaling pathway and negatively correlated with the expression of E-cadherin. Furthermore, CDCA7 transcriptionally regulated the expression of Smad4 and Smad7. Knockdown of CDCA7 inhibited the TGF-β signaling pathway and therefore inhibited EMT. Our data indicated that CDCA7 was heavily involved in EMT by regulating the expression of Smad4 and Smad7 in TGF-β signaling pathway. CDCA7 might be a new therapeutic target in the suppression of metastasis and invasion of ESCC.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaCadherinsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansNuclear ProteinsSmad4 ProteinSmad7 ProteinTransforming Growth Factor betaVimentinCadherinsCDCA7 protein, humanNuclear ProteinsSmad4 ProteinSMAD4 protein, humanSmad7 ProteinSMAD7 protein, humanTransforming Growth Factor betaVimentinCDCA7EMTESCCSmad4/Smad7TGF-β signaling pathway

Identifiers

PMID36056599
PMCPMC9807500
OpenAlexW4294368580

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.