PMID- 34553218
OWN - NLM
STAT- MEDLINE
DCOM- 20220218
LR  - 20220218
IS  - 1745-7270 (Electronic)
IS  - 1672-9145 (Linking)
VI  - 53
IP  - 11
DP  - 2021 Nov 10
TI  - Oct4 downregulation-induced inflammation increases the migration and invasion 
      rate of oral squamous cell carcinoma.
PG  - 1440-1449
LID - 10.1093/abbs/gmab127 [doi]
AB  - Inflammatory changes are involved in tumor cell proliferation, migration, and 
      invasion. Tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS) play 
      important roles in inflammatory regulation during tumor development. Oct4 acts as 
      a transcription factor that modulates inflammatory changes in mesenchymal stem 
      cells. In this study, we explored the role of Oct4 in the invasion and migration 
      of oral squamous cell carcinoma (OSCC) cells. LPS and TNF-alpha were used to treat 
      the OSCC cell lines HN4 and CAL27 to induce inflammation. The generation of 
      inflammatory cytokines, including TNF-alpha, interleukin (IL)-1beta, and IL-6, was 
      evaluated by enzyme-linked immunosorbent assay and real-time quantitative PCR. 
      Western blot analysis was employed to detect the expression and phosphorylation 
      of JNK1, p65, and STAT3, which are key modulators of inflammation. Wound scratch 
      healing and transwell invasion assays were further used to determine the role of 
      inflammation in the invasion and migration of OSCC cells. Robust inflammation was 
      observed in HN4 and CAL27 cells treated with LPS and TNF-alpha. A marked increase in 
      JNK1, p65, and STAT3 phosphorylation levels in OSCC cells was also detected after 
      LPS and TNF-alpha treatment. The migration and invasion of HN4 and CAL27 cells were 
      significantly boosted by stimulation with LPS and TNF-alpha. Furthermore, Oct4 mRNA 
      and protein levels were significantly upregulated by stimulation with LPS and 
      TNF-alpha. Silencing of Oct4 led to reduced inflammation and decreased levels of 
      phosphorylated JNK1, p65, and STAT3 and impaired invasion and migration in LPS- 
      and TNF-alpha-stimulated OSCC cells. Overall, LPS- and TNF-alpha-induced inflammation 
      suppressed the migration and invasion of OSCC cells by upregulating Oct4 
      expression.
CI  - (c) The Author(s) 2021. Published by Oxford University Press on behalf of the 
      Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences. All 
      rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
FAU - Sun, Shuntao
AU  - Sun S
AD  - Department of Stomatology, Tongde Hospital of Zhejiang Province, Hangzhou 310012, 
      China.
FAU - Yang, Hongyu
AU  - Yang H
AD  - Department of Stomatology, Shenzhen Hospital, Peking University, Shenzhen 518035, 
      China.
FAU - Wang, Feng
AU  - Wang F
AD  - Department of Stomatology, Shenzhen Hospital, Peking University, Shenzhen 518035, 
      China.
FAU - Zhao, Shanshan
AU  - Zhao S
AUID- ORCID: 0000-0002-4253-9333
AD  - Department of Stomatology, Tongde Hospital of Zhejiang Province, Hangzhou 310012, 
      China.
LA  - eng
GR  - Tongde Hospital of Zhejiang Province/
PT  - Journal Article
PL  - China
TA  - Acta Biochim Biophys Sin (Shanghai)
JT  - Acta biochimica et biophysica Sinica
JID - 101206716
RN  - 0 (IL1B protein, human)
RN  - 0 (IL6 protein, human)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Octamer Transcription Factor-3)
RN  - 0 (POU5F1 protein, human)
RN  - 0 (RELA protein, human)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 8)
SB  - IM
MH  - Cell Line, Tumor
MH  - Cell Movement/drug effects
MH  - Cell Proliferation/drug effects
MH  - Diffusion Chambers, Culture
MH  - Epithelial Cells/*drug effects/metabolism/pathology
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Inflammation
MH  - Interleukin-1beta/genetics/metabolism
MH  - Interleukin-6/genetics/metabolism
MH  - Lipopolysaccharides/*pharmacology
MH  - Mitogen-Activated Protein Kinase 8/genetics/metabolism
MH  - Models, Biological
MH  - Octamer Transcription Factor-3/antagonists & inhibitors/*genetics/metabolism
MH  - Phosphorylation/drug effects
MH  - *Protein Processing, Post-Translational
MH  - RNA, Small Interfering/genetics/metabolism
MH  - STAT3 Transcription Factor/genetics/metabolism
MH  - Signal Transduction
MH  - Transcription Factor RelA/genetics/metabolism
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism/*pharmacology
OTO - NOTNLM
OT  - Oct4
OT  - inflammation
OT  - invasion
OT  - migration
OT  - oral squamous cell carcinoma (OSCC)
EDAT- 2021/09/24 06:00
MHDA- 2022/02/19 06:00
CRDT- 2021/09/23 06:59
PHST- 2021/03/26 00:00 [received]
PHST- 2021/09/24 06:00 [pubmed]
PHST- 2022/02/19 06:00 [medline]
PHST- 2021/09/23 06:59 [entrez]
AID - 6374278 [pii]
AID - 10.1093/abbs/gmab127 [doi]
PST - ppublish
SO  - Acta Biochim Biophys Sin (Shanghai). 2021 Nov 10;53(11):1440-1449. doi: 
      10.1093/abbs/gmab127.