Evidence map›Paper›PMID 34802034›Full record

ArticleOncogene2022

The interaction between S100A2 and KPNA2 mediates NFYA nuclear import and is a novel therapeutic target for colorectal cancer metastasis.

Fengyan Han, Lei Zhang, Shaoxia Liao, Yanmin Zhang, Lili Qian, Feijun Hou, Jingwen Gong, Maode Lai, Honghe Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 31 citations in OpenAlex.

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  5. E2F7 targets S100A2 to suppress CD8Journal of molecular medicine (Berlin, Germany) · 2026
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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.

Fengyan Han *Department of Pathology and Women's Hospital, Zhejiang University School of Medicine, Research Unit of Intelligence Classification of Tumor Pathology and Precision Therapy, Chinese Academy of Medical Sciences (2019RU042), Hangzhou, 310058, Zhejiang, China.
Lei Zhang *Key Laboratory of Disease Proteomics of Zhejiang Province, Hangzhou, 310058, Zhejiang, China.
Shaoxia LiaoDepartment of Pathology and Women's Hospital, Zhejiang University School of Medicine, Research Unit of Intelligence Classification of Tumor Pathology and Precision Therapy, Chinese Academy of Medical Sciences (2019RU042), Hangzhou, 310058, Zhejiang, China.
Yanmin ZhangLaboratory of Molecular Design and Drug Discovery, School of Science, China Pharmaceutical University, 639 Longmian Avenue, Nanjing, 211198, China.
Lili QianDepartment of Pathology and Women's Hospital, Zhejiang University School of Medicine, Research Unit of Intelligence Classification of Tumor Pathology and Precision Therapy, Chinese Academy of Medical Sciences (2019RU042), Hangzhou, 310058, Zhejiang, China.
Feijun HouDepartment of Pathology and Women's Hospital, Zhejiang University School of Medicine, Research Unit of Intelligence Classification of Tumor Pathology and Precision Therapy, Chinese Academy of Medical Sciences (2019RU042), Hangzhou, 310058, Zhejiang, China.
Jingwen GongKey Laboratory of Disease Proteomics of Zhejiang Province, Hangzhou, 310058, Zhejiang, China.
Maode LaiKey Laboratory of Disease Proteomics of Zhejiang Province, Hangzhou, 310058, Zhejiang, China. lmp@zju.edu.cn.
Honghe ZhangDepartment of Pathology and Women's Hospital, Zhejiang University School of Medicine, Research Unit of Intelligence Classification of Tumor Pathology and Precision Therapy, Chinese Academy of Medical Sciences (2019RU042), Hangzhou, 310058, Zhejiang, China. honghezhang@zju.edu.cn.ORCID http://orcid.org/0000-0001-5954-2857
Chinese Academy of Medical Sciences & Peking Union Medical College · CNChina Pharmaceutical University · CNZhejiang Cancer Hospital · CNZhejiang Chinese Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nucleocytoplasmic transport of proteins is disrupted and dysregulated in cancer cells. Nuclear pore complexes and cargo proteins are two main transportation regulators. However, the mechanism regulating nucleocytoplasmic transport in cancer remains elusive. Here, we identified a S100A2/KPNA2 cotransport complex that transports the tumor-associated transcription factor NFYA in colorectal cancer (CRC). Through the S100A2/KNPA2 complex, depending on its interaction with S100A2, NFYA is transported to the nucleus and inhibits the transcriptional activity of E-cadherin, which in turn promotes CRC metastasis. Targeting the S100A2/KPNA2 binding sites with the specific inhibitor delanzomib is a potential therapeutic approach for CRC.

Indexed as

Active Transport, Cell Nucleusalpha KaryopherinsColorectal NeoplasmsS100 ProteinsAnimalsCadherinsCell Line, TumorCell NucleusChemotactic FactorsGene Expression Regulation, NeoplasticHumansMiceNeoplasm Metastasisalpha KaryopherinsCadherinsChemotactic FactorsKPNA2 protein, humanS100A2 protein, humanS100 Proteins

Identifiers

PMID34802034
OpenAlexW3216843403

What OpenQuestion holds

Textmetadata
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.