Evidence map›Paper›PMID 32181526›Full record

ArticleMolecular carcinogenesis2020

CPNE1 predicts poor prognosis and promotes tumorigenesis and radioresistance via the AKT singling pathway in triple-negative breast cancer.

Zhihong Shao, Xiaolong Ma, Yufeng Zhang, Yuanyuan Sun, Wenjuan Lv, Kuigang He, Rui Xia, Peijun Wang, Xiaolong Gao

Open access · hybridAbstract read
In one paragraph

Article in Molecular carcinogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 69 citations in OpenAlex.

  1. TheInternational journal of molecular sciences · 2021
    Trial
  2. Article
  3. Materials today. Bio · 2026
    Article
  4. Article
  5. Breast cancer (Dove Medical Press) · 2026
    Article
  6. Genes Associated with Apoptosis in an Experimental Breast Cancer Model.International journal of molecular sciences · 2025
    Article
  7. Article
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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 2 institutions in 1 country.

Zhihong ShaoDepartment of Radiology, Shibei hospital of Jing'an District of Shanghai, Shanghai, China.
Xiaolong MaDepartment of Radiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China.
Yufeng ZhangDepartment of Radiology, Luodian Hospital, Shanghai, China.
Yuanyuan SunDepartment of Radiology, Luodian Hospital, Shanghai, China.
Wenjuan LvDepartment of Radiology, Luodian Hospital, Shanghai, China.
Kuigang HeDepartment of Radiology, Luodian Hospital, Shanghai, China.
Rui XiaDepartment of Radiology, Luodian Hospital, Shanghai, China.
Peijun WangDepartment of Radiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China.
Xiaolong GaoDepartment of Radiology, Luodian Hospital, Shanghai, China.ORCID 0000-0002-9911-1776
Tongji University · CNShanghai Zhabei District Shibei Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated expression of Copine 1 (CPNE1) has been observed in multiple cancers; however, the underlying mechanisms by which it affects cancer cells are unclear. We aimed to study the effect of CPNE1 on the tumorigenesis and radioresistance of triple-negative breast cancer (TNBC). Quantitative real-time polymerase chain reaction was used to detect the expression of CPNE1 in TNBC tissues and cell lines. Western blot, immunohistochemistry, and immunofluorescence were used to investigate the levels of CPNE1, p-AKT, AKT, cleaved caspase-3, cleaved PARP1, and γ-H2AX. Cell viability and apoptosis were measured by CCK-8 and flow cytometry, respectively. CPNE1 was overexpressed in TNBC tissues and cell lines and was associated with tumor size, distant metastases, and survival rates of patients with TNBC. Moreover, function study shows that CPNE1 promoted cell viability and inhibited cell apoptosis in vitro and inhibited the radiosensitivity of TNBC. Importantly, inactivation of AKT signaling inhibited the tumorigenesis and radioresistance mediated by CPNE1 in TNBC cells. In vivo xenograft study also shows that CPNE1 knockdown inhibited tumor growth and promoted cell apoptosis. Overall, our findings suggest that CPNE1 promotes tumorigenesis and radioresistance in TNBC by regulating AKT activation and targeted CPNE1 expression may be a strategy to sensitize TNBC cells toward radiation therapy.

Indexed as

Cell ProliferationRadiation ToleranceAnimalsApoptosisBiomarkers, TumorCalcium-Binding ProteinsCohort StudiesFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansMice, NudeMiddle AgedNeoplasm InvasivenessPrognosisProto-Oncogene Proteins c-aktAKT1 protein, humanBiomarkers, TumorCalcium-Binding ProteinsCPNE1 protein, humanProto-Oncogene Proteins c-aktAKTCPNE1DNA damageradioresistancetriple-negative breast cancer

Identifiers

PMID32181526
PMCPMC7187273
OpenAlexW3010670066

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.