Publication: Silencing of SETD6 inhibits the
tumorigenesis of oral squamous cell
carcinoma by inhibiting methylation of PAK4 and RelA
Authors
Huang, Wentao ; Liu, Hongjing ; Lv, Tianzhu
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-327
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info:eu-repo/semantics/article
Description
Abstract
. Background. Oral squamous cell carcinoma
(OSCC) is one of the most comment types of oral
malignancies. SET-domain-containing protein 6
(SETD6) was recently identified as an important
regulator of multiple signaling pathways through
methylating protein substrates. Meanwhile, SETD6 is
known to participate in multiple cancers. However, the
role of SETD6 in OSCC remains unclear.
Methods. Gene and protein expressions in OSCC
cells or tissues were detected by RT-qPCR and western
blot, respectively. In addition, CCK-8 assay was used to
test the cell viability. A transwell assay was performed to
measure cell migration and invasion. Flow cytometry
was used to test cell apoptosis and cycle. Meanwhile,
methylation-specific PCR (MSP) was used to detect the
status of promoter methylation.
Results. SETD6 was significantly upregulated in
OSCC tissues. In addition, knockdown of SETD6
notably inhibited the proliferation and induced the
apoptosis of OSCC cells. Furthermore, silencing of
SETD6 notably suppressed the migration and invasion
of OSCC cells. Meanwhile, SETD6 siRNA significantly
inhibited the promoter methylation of RelA (NF-κB p65)
and PAK4. Furthermore, SETD6 siRNA induced G1
arrest in OSCC cells.
Conclusion. Knockdown of SETD6 inhibits the
tumorigenesis of OSCC by suppressing promoter
methylation of PAK4 and RelA. Therefore, our study
might shed new light on exploring strategies for the
treatment of OSCC.
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Citation
Histology and Histopathology Vol. 36, nº2 (2021)
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