NID1 promotes laryngeal cancer stemness via activating WNT pathway

Bibliographic Details
Title: NID1 promotes laryngeal cancer stemness via activating WNT pathway
Authors: Wenlin Liu, Jie Wu, Yuanpu Lai, Siyi Zhang, Ankui Yang, Yixuan Li, Cuifang Chen, Zhongming Lu
Source: Biology Direct, Vol 19, Iss 1, Pp 1-11 (2024)
Publisher Information: BMC, 2024.
Publication Year: 2024
Collection: LCC:Biology (General)
Subject Terms: NID1, Laryngeal cancer, Radiotherapy resistance, WNT pathway, Cancer stem cells, Biology (General), QH301-705.5
More Details: Abstract Background Laryngeal cancer (LCA) is one of the most common head and neck squamous cell carcinoma with poor outcome. LCA stem cells are the main reason for LCA therapy resistance and relapse. Understanding the molecular mechanisms of the self-renew of LCA stem cells is critical to develop now targets and strategies for LCA therapy. Methods Q-PCR and western blotting assays were used to determine NID1 level in LCA tissues and normal laryngeal tissues. MTT, colony formation assay, apoptosis assay and animal model were used to investigate the effect of NID1 on radiotherapy resistance. Side population assay and sphere formation assay were used to determine the role of LCA in the self-renew of LCA stem cells. Results NID1 was upregulated in LCA tissues, particularly in LCA tissues derived from relapsed patients, and associated with had poor outcome. NID1 knockdown suppressed radiotherapy resistance and the self-renew of LCA stem cells, while NID1 overexpression promoted radiotherapy resistance and the self-renew of LCA stem cells. Further analysis showed that NID1 promotes radiotherapy resistance and the self-renew of LCA stem cells via activating WNT pathway. Moreover, NID1 level was positively correlated with nuclear β-Catenin level in LCA tissues. Conclusion Our results show that NID1 promotes radiotherapy resistance and the self-renew of LCA stem cells via activating WNT pathway, providing a novel potential target for LCA treatment.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1745-6150
50563718
Relation: https://doaj.org/toc/1745-6150
DOI: 10.1186/s13062-024-00548-0
Access URL: https://doaj.org/article/0f505637185844af98c4023ce0b8991d
Accession Number: edsdoj.0f505637185844af98c4023ce0b8991d
Database: Directory of Open Access Journals
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More Details
ISSN:17456150
50563718
DOI:10.1186/s13062-024-00548-0
Published in:Biology Direct
Language:English