Evidence map›Paper›PMID 40000619›Full record

ArticleCell death discovery2025

NFIX suppresses breast cancer cell proliferation by delaying mitosis through downregulation of CDK1 expression.

Hai-Yan Ma, Rui Sun, Tian Tian, Xue-Jie Zhou, Zhao-Hui Chen, Xu-Chen Cao, Yue Yu, Xin Wang

Abstract read
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Dynamic NFIX Promoter Usage Shapes Stem and Committed Myogenic States.International journal of molecular sciences · 2026
    Article
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  3. Article
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  5. [Nuclear Factor I-X Regulates Molecular Pathways Related to Craniofacial Development Through Phase Separation].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025
    Article
  6. Article
  7. Article
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

8 authors.

Hai-Yan Ma *The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Rui Sun *The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Tian Tian *The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Xue-Jie ZhouThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Zhao-Hui ChenThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Xu-Chen CaoThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Yue YuThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China. yuyue@tmu.edu.cn.ORCID http://orcid.org/0000-0003-2053-9866
Xin WangThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China. wangxin@tjmuch.com.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82172827National Natural Science Foundation of China (National Science Foundation of China) 82172835
6 · The paper itself

Abstract

One of the fundamental biological characteristics of malignant tumors is their uncontrolled growth and multiplication, which is a major reason why breast cancer remains incurable. The significance of NFIX in the development of various cancers has been demonstrated by an increasing number of studies in recent years. However, the role of NFIX in breast cancer has received less attention. This study investigates its expression in breast cancer and its function in inhibiting cell cycle progression. NFIX is downregulated in breast cancer compared to normal breast tissue, which impacts prognosis. In vitro and in vivo Experiments have shown that the overexpression of NIFX leads to a delay in the G2/M phase, which inhibits breast cancer cell proliferation. It thus plays a role as a tumor suppressor in breast cancer development. In terms of mechanism, upregulating NFIX causes CDK1 to be more susceptible to ubiquitination-mediated degradation. NFIX also competitively represses CDK1 transcription via YBX1. Moreover, NFIX expression in breast cancer is associated with methylation of its promoter region. Our study demonstrated that NFIX plays a critical role in CDK1-regulated cell cycle transitions and determined that NFIX inhibits cell proliferation in breast cancer.

Identifiers

PMID40000619
PMCPMC11861311

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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.