MTSS1 is downregulated in nasopharyngeal carcinoma (NPC) which disrupts adherens junctions leading to enhanced cell migration and invasion

被引:1
作者
Zheng, Shixing [1 ,2 ,3 ]
Wang, Xiaoxia [1 ]
Matskova, Liudmila [1 ]
Zhou, Xiaoying [4 ]
Zhang, Zhe [5 ]
Kashuba, Elena [1 ,6 ]
Ernberg, Ingemar [1 ]
Aspenstrom, Pontus [1 ,7 ]
机构
[1] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden
[2] Fudan Univ, ENT Inst, Shanghai, Peoples R China
[3] Fudan Univ, Eye & ENT Hosp, Dept Otorhinolaryngol, Shanghai, Peoples R China
[4] Guangxi Med Univ, Life Sci Inst, Sci Res Ctr, Nanning, Peoples R China
[5] Guangxi Med Univ, Dept Otolaryngol Head & Neck Surg, Affiliated Hosp 1, Nanning, Peoples R China
[6] Natl Acad Sci Ukraine, RE Kavetsky Inst Expt Pathol Oncol & Radiobiol, Kiev, Ukraine
[7] Uppsala Univ, Dept Immunol Genet & Pathol, Rudbeck Lab, Uppsala, Sweden
来源
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY | 2023年 / 11卷
基金
中国国家自然科学基金;
关键词
invasion; metastasis; MTSS1; nasopharyngeal carcinoma; adherens junctions; I-BAR domain; ACTIN; MIM; METASTASIS; CANCER; SUPPRESSOR; EXPRESSION; PROTEIN; GENE;
D O I
10.3389/fcell.2023.1275668
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Loss of cell-cell adhesions is the indispensable first step for cancer cells to depart from the primary tumor mass to metastasize. Metastasis suppressor 1 (MTSS1) is frequently lost in metastatic tissues, correlating to advanced tumor stages and poor prognosis across a variety of cancers. Here we explore the anti-metastatic mechanisms of MTSS1, which have not been well understood. We found that MTSS1 is downregulated in NPC tissues. Lower levels of MTSS1 expression correlate to worse prognosis. We show that MTSS1 suppresses NPC cell migration and invasion in vitro through cytoskeletal remodeling at cell-cell borders and assembly of E-cadherin/beta-catenin/F-actin in adherens junctions. The I-BAR domain of MTSS1 was both necessary and sufficient to restore this formation of E-cadherin/beta-catenin/F-actin-mediated cell adherens junctions.
引用
收藏
页数:13
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