Evidence map›Paper›PMID 35348268›Full record

ArticleCancer science2023

NCAPD2 promotes breast cancer progression through E2F1 transcriptional regulation of CDK1.

Jinsong He, Rui Gao, Jianbo Yang, Feng Li, Yang Fu, Junwei Cui, Xiaoling Liu, Kanghua Huang, Qiuyi Guo, Zihan Zhou and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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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

11 authors at 2 institutions in 2 countries.

Jinsong HeDepartment of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.ORCID https://orcid.org/0000-0002-0850-5260
Rui GaoDepartment of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Jianbo YangDepartment of The Cancer Center, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
Feng LiDepartment of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Yang FuDepartment of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Junwei CuiDepartment of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Xiaoling LiuDepartment of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Kanghua HuangDepartment of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Qiuyi GuoDepartment of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Zihan ZhouDepartment of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Wei WeiDepartment of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Peking University Shenzhen Hospital · CNFujian Medical University · CN

Funding

Research Foundation of University Shenzhen HospitalShenzhen High-Level Hospital Struction FundShenzhen International Cooperation Research Project (with University of Minnesota cooperation) GJHZ20180928115030292Shenzhen Key Medical Discipline Construction Fund SZXK017Shenzhen San-ming Project SZSM201612010
6 · The paper itself

Abstract

Breast cancer (BC) is a serious threat to women's health worldwide. Non-SMC condensin I complex subunit D2 (NCAPD2) is a regulatory subunit of the coagulin I complex, which is mainly involved in chromosome coagulation and separation. The clinical significance, biological behavior, and potential molecular mechanism of NCAPD2 in BC were investigated in this study. We found that NCAPD2 was frequently overexpressed in BC, and it had clinical significance in predicting the prognosis of BC patients. Moreover, loss-of-function assays demonstrated that NCAPD2 knockdown restrained the progression of BC by inhibiting proliferation and migration and enhancing apoptosis in vitro. It was further confirmed that the downregulation of NCAPD2 inhibited tumor growth in vivo. NCAPD2 promoted the progression of BC through the extracellular signal-regulated kinase 5 (ERK5) signaling pathway. Additionally, NCAPD2 could transcriptionally activate CDK1 by interacting with E2F transcription factor 1 (E2F1) in MDA-MB-231 cells. Overexpression of CDK1 alleviated the inhibitory effects of NCAPD2 knockdown in BC cells. In summary, the NCAPD2/E2F1/CDK1 axis may play a role in promoting the progression of BC, which may provide a blueprint for molecular therapy.

Indexed as

Breast NeoplasmsCDC2 Protein KinaseCell Line, TumorCell ProliferationChromosomal Proteins, Non-HistoneDown-RegulationE2F1 Transcription FactorFemaleGene Expression Regulation, NeoplasticHumansPoly-ADP-Ribose Binding ProteinsSignal TransductionCDC2 Protein KinaseCDK1 protein, humanChromosomal Proteins, Non-HistoneE2F1 protein, humanE2F1 Transcription FactorNCAPD2 protein, humanPoly-ADP-Ribose Binding ProteinsBCCDK1migrationNCAPD2proliferationtranscriptional regulation

Identifiers

PMID35348268
PMCPMC9986070
OpenAlexW4221078247

What Socratic 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 Socratic graph.