Publication: Upregulation of LY6K induced by FTO-mediated demethylation promotes the tumorigenesis and metastasis of oral squamous cell carcinoma via CAV-1-mediated ERK1/2 signaling activation
Authors
Xu, Chen ; Gong, Rujuan ; Yang, Haibing
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Publisher
Universidad de Murcia. Departamento de BiologĂa Celular e HistologĂa
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DOI
https://doi.org/10.14670/HH-18-725
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info:eu-repo/semantics/article
Description
Abstract
Lymphocyte antigen 6 complex locus K
(LY6K) has been demonstrated to play a significant role
in cancers and identified as a therapeutic biomarker for
head and neck squamous cell carcinoma. However, the
role of LY6K in oral squamous cell carcinoma (OSCC)
has not been explored. The current study discovered that
LY6K was aberrantly upregulated in OSCC cell lines
and tissues and that high LY6K expression significantly
correlated with poorer survival of OSCC patients.
Through stable knockdown of LY6K, we found that the
growth, colony formation, migration, and invasion of
OSCC cells were substantially suppressed. In addition,
tumor growth and lung metastasis in vivo were
effectively inhibited by LY6K depletion. Mechanically,
LY6K binds with CAV-1 and activates CAV-1-mediated
MAPK/ERK signaling to exert its oncogenic effects on
OSCC. In addition, LY6K expression in OSCC was
discovered to be regulated by FTO-mediated RNA N6-
methyladenosine (m6A) modification in an IGF2BP1-
dependent manner. Generally, LY6K expression was
upregulated by FTO-mediated demethylation in OSCC,
which promoted the tumorigenesis and metastasis of
OSCC via activating the CAV-1-mediated ERK1/2
signaling pathway
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Citation
Histology and Histopathology, Vol.39, nÂş10, (2024)
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