Evidence map›Paper›PMID 33816467›Full record

ArticleFrontiers in cell and developmental biology2021

ATF3 Suppresses Growth and Metastasis of Clear Cell Renal Cell Carcinoma by Deactivating EGFR/AKT/GSK3β/β-Catenin Signaling Pathway.

Shenglin Gao, Lei Gao, Simin Wang, Xiaokai Shi, Chuang Yue, Shuzhang Wei, Li Zuo, Lifeng Zhang, Xihu Qin

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. 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
1.1field-weighted citation impact, top 24% 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, 16 citations in OpenAlex.

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  8. Induction of heparanase 2 (Hpa2) expression by stress is mediated by ATF3.Matrix biology : journal of the International Society for Matrix Biology · 2022
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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

9 authors at 4 institutions in 1 country.

Shenglin GaoDepartment of Urology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Lei GaoDepartment of Urology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Simin WangChangzhou Third People's Hospital, Changzhou, China.
Xiaokai ShiDepartment of Urology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Chuang YueDepartment of Urology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Shuzhang WeiDepartment of Urology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Li ZuoDepartment of Urology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Lifeng ZhangDepartment of Urology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Xihu QinDepartment of General Surgery, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Changzhou No.2 People's Hospital · CNNanjing Medical University · CNChangzhou Third People's Hospital · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClear cell renal cell carcinoma (ccRCC) is one of the most common malignant cancers in East Asia, with high incidence and mortality. Accumulating evidence has shown that ATF3 is associated with tumor progression.

methodsUsing qPCR, the expression of ATF3 was detected in 93 patients with ccRCC, including 24 paired normal and tumor tissues, which were used to further compare ATF3 expression through western blotting and immunohistochemistry. Lentivirus was used for the overexpression or knockdown of ATF3, and the consequent alteration in function was analyzed through CCK8 assay, colony formation assay, wound healing assay, invasion assay, and flow cytometry. The potential mechanism affected by ATF3 was analyzed through gene set enrichment analysis (GSEA) and verified using western blotting, invasion assay, or immunofluorescence staining. Furthermore, a xenograft mouse model was used to assess the function of ATF3

resultsATF3 expression was significantly decreased in ccRCC compared to that in adjacent normal tissues. Through gain- and loss-of-function experiments performed in an

conclusionATF3 could be utilized as an independent protective factor to inhibit the progression of ccRCC. Potential treatment strategies for ccRCC include targeting the ATF3/EGFR/AKT/GSK3β/β-catenin signaling pathway.

Indexed as

activation transcription factor 3clear cell renal cell carcinomagrowthGSEAmetastasis

Identifiers

PMID33816467
PMCPMC8017234
OpenAlexW3139392707

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.