Roles of IGFBP-3 in cell migration and growth in an endophytic tongue squamous cell carcinoma cell line

Insulin-like growth factor binding protein-3 (IGFBP-3) is a member of the IGFBP family that has high affinity for IGFs and functions as either an oncogene or tumor suppressor in various types of cancer. We previously found that IGFBP3 mRNA levels are higher in endophytic-type human tongue squamous c...

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Bibliographic Details
Published in:Scientific reports 2022-07, Vol.12 (1), p.11503-11503, Article 11503
Main Authors: Ng, Esther Feng Ying, Kaida, Atsushi, Nojima, Hitomi, Miura, Masahiko
Format: Article
Language:English
Subjects:
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631/67/1665
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631/80/86/2368
Cell adhesion & migration
Cell cycle
Cell migration
Endophytes
Humanities and Social Sciences
Insulin
Insulin-like growth factor-binding protein 3
Invasiveness
Metastases
mRNA
multidisciplinary
Oral cancer
Science
Science (multidisciplinary)
Sequence analysis
Squamous cell carcinoma
Tongue
Tumor suppressor genes
Tumors
Ubiquitination
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Summary:Insulin-like growth factor binding protein-3 (IGFBP-3) is a member of the IGFBP family that has high affinity for IGFs and functions as either an oncogene or tumor suppressor in various types of cancer. We previously found that IGFBP3 mRNA levels are higher in endophytic-type human tongue squamous cell carcinoma (TSCC) that is more invasive and more prone to metastasis than exophytic and superficial types. This finding prompted us to investigate the roles of IGFBP-3 in TSCC using SAS cells, which were originally derived from endophytic-type TSCC. Specifically, we used SAS cells that express a fluorescent ubiquitination-based cell-cycle indicator (Fucci). RNA-sequencing analysis indicated that IGFBP-3 is associated with cell migration and cell growth. In fact, IGFBP-3 knockdown downregulates cell migration and causes cells to arrest in G 1 . This migratory potential appears to be cell cycle–independent. IGFBP-3 knockdown also reduced levels of secreted IGFBP-3; however, decreased migratory potential was not rescued by exogenous recombinant human IGFBP-3. Furthermore, ERK activity was downregulated by IGFBP-3 depletion, which suggests that MEK/ERK signaling may be involved in IGFBP-3-mediated cell migration. We therefore conclude that intracellular IGFBP-3 enhances cell migration independently of the cell cycle in TSCC with a higher metastatic potential.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-022-15737-y