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Peer-reviewedCC BY 4.0Cancers

YY1 Suppresses Tumor Growth by Negatively Regulating the Expression and Translation Activity of eIF4E in Nasopharyngeal Carcinoma

  • Yumei Duan1,2,3,4
  • Xiangting Zhou1,2,3
  • Jianxia Wei1,2,3
  • Changning Xue1,2,3
  • Lemei Zheng1,2,3
  • Ting Zeng1,2,3
  • Hongyu Deng1,2
  • Songqing Fan5
  • Wei Xiong1,2,3
  • Ming Zhou1,2,3
  • Shuping Peng1,2,3
  • Mengna Li1,2,3
5 affiliations
  1. 1NHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China
  2. 2Cancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha 410078, China
  3. 3The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Central South University, Changsha 410078, China
  4. 4Department of Pathology, Xiangya Hospital, Central South University, Changsha 410008, China
  5. 5Department of Pathology, The Second Xiangya Hospital, Central South University, Changsha 410011, China
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Abstract

Background: Nasopharyngeal carcinoma (NPC) is a complex malignancy, and the molecular mechanisms that drive its progression have not yet been fully elucidated. Eukaryotic translation initiation factor 4E (eIF4E), a pivotal regulator of protein synthesis, is frequently dysregulated in cancers. We previously identified eIF4E as a direct transcriptional target of Yin Yang 1 (YY1) in an axis where YY1 suppressed NPC invasion and metastasis. Methods: Here, we investigated the function of eIF4E in NPC growth and its regulatory relationship with YY1. The CCK-8 assay, clonogenic survival assay, Annexin V/propidium iodide assay, and xenograft models were used to determine the role of YY1/eIF4E in NPC growth; Western blotting and Co-IP were performed to examine protein expression and protein–protein interactions, respectively. Results: Our findings demonstrate that eIF4E potently promoted NPC cell proliferation, accelerated cell cycle progression, and inhibited apoptosis. Moreover, these effects were critically dependent on its phosphorylation at serine 209 (S209). Furthermore, we uncovered a novel regulatory mechanism whereby YY1 enhances the association between 4E-BP1 and eIF4E, downregulates eIF4G expression, and is associated with reduced interaction between eIF4E and eIF4G, thereby potentially limiting eIF4F complex formation. Conclusions: This study establishes eIF4E phosphorylation as an oncogenic driver of NPC cell growth and survival and identifies YY1 as a tumor suppressor that negatively regulates this axis. These insights position eIF4E as a promising and precise therapeutic target for NPC intervention.

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Cite

BibTeXRIS
BibTeX
@article{duan2026suppresses,
  title = {{YY1 Suppresses Tumor Growth by Negatively Regulating the Expression and Translation Activity of eIF4E in Nasopharyngeal Carcinoma}},
  author = {Yumei Duan and Xiangting Zhou and Jianxia Wei and Changning Xue and Lemei Zheng and Ting Zeng and Hongyu Deng and Songqing Fan and Wei Xiong and Ming Zhou and Shuping Peng and Mengna Li},
  journal = {Cancers},
  year = {2026},
  month = oct,
  doi = {10.3390/cancers18203257},
  url = {https://www.mdpi.com/2072-6694/18/20/3257},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - YY1 Suppresses Tumor Growth by Negatively Regulating the Expression and Translation Activity of eIF4E in Nasopharyngeal Carcinoma
AU  - Yumei Duan
AU  - Xiangting Zhou
AU  - Jianxia Wei
AU  - Changning Xue
AU  - Lemei Zheng
AU  - Ting Zeng
AU  - Hongyu Deng
AU  - Songqing Fan
AU  - Wei Xiong
AU  - Ming Zhou
AU  - Shuping Peng
AU  - Mengna Li
PY  - 2026
DA  - 2026/10/01
JO  - Cancers
DO  - 10.3390/cancers18203257
UR  - https://www.mdpi.com/2072-6694/18/20/3257
AB  - Background: Nasopharyngeal carcinoma (NPC) is a complex malignancy, and the molecular mechanisms that drive its progression have not yet been fully elucidated. Eukaryotic translation initiation factor 4E (eIF4E), a pivotal regulator of protein synthesis, is frequently dysregulated in cancers. We previously identified eIF4E as a direct transcriptional target of Yin Yang 1 (YY1) in an axis where YY1 suppressed NPC invasion and metastasis. Methods: Here, we investigated the function of eIF4E in NPC growth and its regulatory relationship with YY1. The CCK-8 assay, clonogenic survival assay, Annexin V/propidium iodide assay, and xenograft models were used to determine the role of YY1/eIF4E in NPC growth; Western blotting and Co-IP were performed to examine protein expression and protein–protein interactions, respectively. Results: Our findings demonstrate that eIF4E potently promoted NPC cell proliferation, accelerated cell cycle progression, and inhibited apoptosis. Moreover, these effects were critically dependent on its phosphorylation at serine 209 (S209). Furthermore, we uncovered a novel regulatory mechanism whereby YY1 enhances the association between 4E-BP1 and eIF4E, downregulates eIF4G expression, and is associated with reduced interaction between eIF4E and eIF4G, thereby potentially limiting eIF4F complex formation. Conclusions: This study establishes eIF4E phosphorylation as an oncogenic driver of NPC cell growth and survival and identifies YY1 as a tumor suppressor that negatively regulates this axis. These insights position eIF4E as a promising and precise therapeutic target for NPC intervention.
SN  - 2072-6694
ER  -