Bibliographic Details
| Title: |
NFIX suppresses breast cancer cell proliferation by delaying mitosis through downregulation of CDK1 expression |
| Authors: |
Hai-Yan Ma, Rui Sun, Tian Tian, Xue-Jie Zhou, Zhao-Hui Chen, Xu-Chen Cao, Yue Yu, Xin Wang |
| Source: |
Cell Death Discovery, Vol 11, Iss 1, Pp 1-12 (2025) |
| Publisher Information: |
Nature Publishing Group, 2025. |
| Publication Year: |
2025 |
| Collection: |
LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
LCC:Cytology |
| Subject Terms: |
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Cytology, QH573-671 |
| More Details: |
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. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
2058-7716 |
| Relation: |
https://doaj.org/toc/2058-7716 |
| DOI: |
10.1038/s41420-025-02361-8 |
| Access URL: |
https://doaj.org/article/22ca2276eedf4502b700e133b266fb86 |
| Accession Number: |
edsdoj.22ca2276eedf4502b700e133b266fb86 |
| Database: |
Directory of Open Access Journals |
