Bibliographic Details
Title: |
C/EBPβ Regulates HIF-1α-Driven Invasion of Non-Small-Cell Lung Cancer Cells |
Authors: |
Seung Hee Seo, Ji Hae Lee, Eun Kyung Choi, Seung Bae Rho, Kyungsil Yoon |
Source: |
Biomolecules, Vol 15, Iss 1, p 36 (2024) |
Publisher Information: |
MDPI AG, 2024. |
Publication Year: |
2024 |
Collection: |
LCC:Microbiology |
Subject Terms: |
C/EBPβ, hypoxia, HIF-1α, metastasis, non-small-cell lung cancer, Microbiology, QR1-502 |
More Details: |
Metastatic cancer accounts for most cancer-related deaths, and identifying specific molecular targets that contribute to metastatic progression is crucial for the development of effective treatments. Hypoxia, a feature of solid tumors, plays a role in cancer progression by inducing resistance to therapy and accelerating metastasis. Here, we report that CCAAT/enhancer-binding protein beta (C/EBPβ) transcriptionally regulates hypoxia-inducible factor 1 subunit alpha (HIF1A) and thus promotes migration and invasion of non-small-cell lung cancer (NSCLC) cells under hypoxic conditions. Our results show that knockdown or forced expression of C/EBPβ was correlated with HIF-1α expression and that C/EBPβ directly bound to the promoter region of HIF1A. Silencing HIF1A inhibited the enhanced migration and invasion induced by C/EBPβ overexpression in NSCLC cells under hypoxia. Expression of the HIF-1α target gene, SLC2A1, was also altered in a C/EBPβ-dependent manner, and knockdown of SLC2A1 reduced migration and invasion enhanced by C/EBPβ overexpression. These results indicate that C/EBPβ is a critical regulator for the invasion of NSCLC cells in the hypoxic tumor microenvironment. Collectively, the C/EBPβ-HIF-1α-GLUT1 axis represents a potential therapeutic target for preventing metastatic progression of NSCLC and improving patient outcomes. |
Document Type: |
article |
File Description: |
electronic resource |
Language: |
English |
ISSN: |
2218-273X |
Relation: |
https://www.mdpi.com/2218-273X/15/1/36; https://doaj.org/toc/2218-273X |
DOI: |
10.3390/biom15010036 |
Access URL: |
https://doaj.org/article/731975892c074012b6652427ffeac2b2 |
Accession Number: |
edsdoj.731975892c074012b6652427ffeac2b2 |
Database: |
Directory of Open Access Journals |
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