Villin-like protein VILL suppresses proliferation of nasopharyngeal carcinoma cells by interacting with LMO7 protein.
10.12122/j.issn.1673-4254.2025.05.07
- Author:
Yumei ZENG
1
;
Jike LI
2
;
Zhongxi HUANG
2
;
Yibo ZHOU
3
Author Information
1. Department of Pathology, Zhongshan People's Hospital, Zhongshan 528400, China.
2. Cancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
3. Department of Otolaryngology and Head-Neck Surgery, Changsha Hospital of Traditional Chinese Medicine (Changsha Eighth Hospital), Changsha 410010, China.
- Publication Type:Journal Article
- Keywords:
LMO7 protein;
cell proliferation;
nasopharyngeal carcinoma;
protein interaction;
villin-like protein VILL
- MeSH:
Nasopharyngeal Neoplasms/metabolism*;
Humans;
LIM Domain Proteins/metabolism*;
Cell Proliferation;
Cell Line, Tumor;
Animals;
Mice;
Nasopharyngeal Carcinoma;
Mice, Nude;
Transcription Factors/metabolism*;
Carcinoma;
Female;
Microfilament Proteins/genetics*;
Male;
Middle Aged
- From:
Journal of Southern Medical University
2025;45(5):954-961
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To elucidate the molecular mechanism by which villin-like protein VILL (VILL) inhibits proliferation of nasopharyngeal carcinoma (NPC) cells.
METHODS:Co-immunoprecipitation (CO-IP) assay, mass spectrometry, Western blotting, immunofluorescence staining, and GST pull-down assay were employed to identify and confirm the protein interacting with VILL that had the highest abundance in NPC cell lines. Transgenic experiments were conducted in both NPC cell lines and nude mice to validate the regulatory role of VILL and its target protein in NPC proliferation. Immunohistochemistry was utilized to assess the correlation of the expression levels of VILL and its target protein in clinical tissue specimens of NPC with the clinical features of the patients.
RESULTS:In NPC cell lines (HONE1 EBV and S18), VILL was found to interact most abundantly with the E3 ubiquitin ligase LMO7, and both proteins co-localized in the cytoplasm with direct interactions. Overexpression of LMO7 partially counteracted the inhibitory effect of VILL on NPC cell proliferation. The expression of VILL was significantly downregulated in 136 NPC tissue samples compared to 67 non-cancerous nasopharyngeal tissues (P<0.00001) with close correlation with clinical T stage (P=0.04), N stage (P=0.01), and M stage (P=0.013), whereas LMO7 was highly expressed in all the NPC tissues.
CONCLUSIONS:VILL overexpression inhibits NPC proliferation probably by suppressing the oncogenic function of LMO7.
