Evidence map›Paper›PMID 35197448›Full record

ArticleCell death & disease2022

SAPCD2 promotes neuroblastoma progression by altering the subcellular distribution of E2F7.

Zi-Mu Zhang, Hai-Bo Cao, Zhi-Heng Li, Ran Zhuo, Yan-Fang Tao, Xiao-Lu Li, Gen Li, Xin-Mei Liao, Fang Fang, Yi Xie and 13 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

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  13. Nuclear transport proteins: structure, function, and disease relevance.Signal transduction and targeted therapy · 2023
    Review
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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

23 authors at 2 institutions in 1 country.

Zi-Mu Zhang *Institute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.ORCID 0000-0002-7791-4252
Hai-Bo Cao *Institute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Zhi-Heng Li *Institute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Ran Zhuo *Institute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Yan-Fang TaoInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Xiao-Lu LiInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Gen LiInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Xin-Mei LiaoSchool of Electronic Information and Electrical Engineering, Shanghai Jiao Tong University, Shanghai, 200000, China.
Fang FangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Yi XieInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Di WuInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Hai-Rong WangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Jian-Wei WangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Yan-Ling ChenInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Juan-Juan YuInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Si-Qi JiaInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Ran-Dong YangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Xin-Yi GuoMedical College of Soochow University, Suzhou, 215123, Jiangsu, China.
Yang YangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Chen-Xi FengInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Yun-Yun XuInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China.
Guang-Hui QianInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China. ghqian@suda.edu.cn.ORCID 0000-0002-9983-8983
Jian PanInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, 215003, Jiangsu, China. panjian2019@suda.edu.cn.ORCID 0000-0002-0292-5141
Soochow University · CNShanghai Jiao Tong University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 52003183National Natural Science Foundation of China (National Science Foundation of China) 81802499National Natural Science Foundation of China (National Science Foundation of China) 81971867National Natural Science Foundation of China (National Science Foundation of China) 82072767National Natural Science Foundation of China (National Science Foundation of China) 82171797
6 · The paper itself

Abstract

Recent studies uncovered the emerging roles of SAPCD2 (suppressor anaphase-promoting complex domain containing 2) in several types of human cancer. However, the functions and underlying mechanisms of SAPCD2 in the progression of neuroblastoma (NB) remain elusive. Herein, through integrative analysis of public datasets and regulatory network of GSK-J4, a small-molecule drug with anti-NB activity, we identified SAPCD2 as an appealing target with a high connection to poor prognosis in NB. SAPCD2 promoted NB progression in vitro and in vivo. Mechanistically, SAPCD2 could directly bind to cytoplasmic E2F7 but not E2F1, alter the subcellular distribution of E2F7 and regulate E2F activity. Among the E2F family members, the roles of E2F7 in NB are poorly understood. We found that an increasing level of nuclear E2F7 was induced by SAPCD2 knockdown, thereby affecting the expression of genes involved in the cell cycle and chromosome instability. In addition, Selinexor (KTP-330), a clinically available inhibitor of exportin 1 (XPO1), could induce nuclear accumulation of E2F7 and suppress the growth of NB. Overall, our studies suggested a previously unrecognized role of SAPCD2 in the E2F signaling pathway and a potential therapeutic approach for NB, as well as clues for understanding the differences in subcellular distribution of E2F1 and E2F7 during their nucleocytoplasmic shuttling.

Indexed as

E2F7 Transcription FactorNeuroblastomaNuclear ProteinsActive Transport, Cell NucleusCell CycleCell Line, TumorCell NucleusHumansE2F7 protein, humanE2F7 Transcription FactorNuclear ProteinsSAPCD2 protein, human

Identifiers

PMID35197448
PMCPMC8866461
OpenAlexW4214749296

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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.