Evidence map›Paper›PMID 35627188›Full record

ArticleGenes2022

Cdh1 Deficiency Sensitizes TNBC Cells to PARP Inhibitors.

Junjun Li, Mengjiao Lan, Jin Peng, Qunli Xiong, Yongfeng Xu, Yang Yang, Ying Zhou, Jinlu Liu, Zhu Zeng, Xiaojuan Yang and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025
    Review
  3. Review
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

14 authors at 2 institutions in 1 country.

Junjun LiDepartment of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu 610000, China.
Mengjiao LanZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital of Zhejiang University, Hangzhou 310003, China.
Jin PengZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital of Zhejiang University, Hangzhou 310003, China.
Qunli XiongDepartment of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu 610000, China.
Yongfeng XuDepartment of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu 610000, China.
Yang YangDepartment of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu 610000, China.
Ying ZhouDepartment of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu 610000, China.
Jinlu LiuDepartment of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu 610000, China.
Zhu ZengDepartment of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu 610000, China.
Xiaojuan YangDepartment of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu 610000, China.
Zhiwei ZhangDepartment of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu 610000, China.
Pumin ZhangZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital of Zhejiang University, Hangzhou 310003, China.
Qing ZhuDepartment of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu 610000, China.ORCID 0000-0003-2182-5709
Wei WuZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital of Zhejiang University, Hangzhou 310003, China.
Sichuan University · CNFirst Affiliated Hospital Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is a type of breast tumor that currently lacks options for targeted therapy. Tremendous effort has been made to identify treatment targets for TNBC. Here, we report that the expression level of anaphase promoting complex (APC) coactivator Cdh1 in TNBC is elevated compared to that in the adjacent healthy tissues, and high levels of Cdh1 expression are correlated with poor prognoses, suggesting that Cdh1 contributes to the progression of TNBC. Interfering with the function of Cdh1 can potentiate the cytotoxic effects of PARP inhibitors against BRCA-deficient and BRCA-proficient TNBC cells through inducing DNA damage, checkpoint activation, cell cycle arrest, and apoptosis. Further investigation reveals that Cdh1 promotes BRCA1 foci formation and prevents untangled DNA entering mitosis in response to PARP inhibition (PARPi) in TNBC cells. Collectively, these results suggest that APC/Cdh1 is a potential molecular target for PARPi-based therapies against TNBCs.

Indexed as

Antineoplastic AgentsTriple Negative Breast NeoplasmsAntigens, CDCadherinsCell Line, TumorDNA DamageHumansPoly(ADP-ribose) Polymerase InhibitorsAntigens, CDAntineoplastic AgentsCadherinsCDH1 protein, humanPoly(ADP-ribose) Polymerase InhibitorsBRCA1Cdh1olaparibPARPtriple-negative breast cancer

Identifiers

PMID35627188
PMCPMC9141497
OpenAlexW4225161394

What Socratic 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 Socratic graph.