PMID- 37948132
OWN - NLM
STAT- MEDLINE
DCOM- 20231113
LR  - 20240229
IS  - 1555-8576 (Electronic)
IS  - 1538-4047 (Print)
IS  - 1538-4047 (Linking)
VI  - 24
IP  - 1
DP  - 2023 Dec 31
TI  - NAT10 promotes the tumorigenesis and progression of laryngeal squamous cell 
      carcinoma through ac4C modification of FOXM1 mRNA.
PG  - 2274143
LID - 10.1080/15384047.2023.2274143 [doi]
LID - 2274143
AB  - Laryngeal squamous cell carcinoma (LSCC), is a prevalent malignant tumor, belongs 
      to the category of head and neck tumors. N-acetyltransferase 10 (NAT10) can alter 
      mRNA stability through N4- acetylcytidine (ac4C) modification. This study aimed 
      to make an investigation into the role of NAT10-mediated ac4C modification in the 
      malignant processes of LSCC cells. The NAT10 expression in LSCC tissues and cells 
      was detected RT-qPCR and western blot. The ac4C dot blot was performed to detect 
      ac4C level. Besides, the cell viability, migration, and invasion abilities were 
      detected by CCK-8 and transwell assays. AcRIP-qPCR was performed to measure the 
      abundance of ac4C on FOXM1 mRNA. RIP and Luciferase reporter assays were 
      performed to demonstrate the interaction between NAT10 and FOXM1. Finally, the 
      xenograft model was established to explore the role of NAT10 in vivo. NAT1 levels 
      were significantly increased in the LSCC tissues and cells. Knockdown of NAT10 
      could significantly suppress the proliferation, migration, and invasion of LSCC 
      cells. Additionally, NAT10 recognized the ac4C-modified sites in the 
      3'-untranslated regions (3' UTR) of forkhead box M1 (FOXM1) to enhance the 
      ability of FOXM1 mRNA. Furthermore, FOXM1 overexpression reversed the suppressing 
      effects of NAT10 knockdown on the proliferation, migration, and invasion of LSCC 
      cells, according to the results of rescue assays. Finally, results of animal 
      experiments showed that NAT10 promoted in vivo tumorigenesis of LSCC cells 
      through upregulating FOXM1. Our current study demonstrated that NAT10-mediated 
      ac4C modification of FOXM1 mRNA promoted the malignant processes of LSCC cells.
FAU - Li, Zengpei
AU  - Li Z
AD  - Department of Otolaryngology, Nanyang First People's Hospital, Nanyang, Henan, 
      China.
FAU - Li, Dajun
AU  - Li D
AD  - Department of Otolaryngology, Nanyang First People's Hospital, Nanyang, Henan, 
      China.
FAU - Yang, Tianbin
AU  - Yang T
AD  - Department of Otolaryngology, Nanyang First People's Hospital, Nanyang, Henan, 
      China.
FAU - Yao, Chen
AU  - Yao C
AUID- ORCID: 0009-0004-1808-7578
AD  - Department of Otolaryngology, Nanyang First People's Hospital, Nanyang, Henan, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20231110
PL  - United States
TA  - Cancer Biol Ther
JT  - Cancer biology & therapy
JID - 101137842
RN  - 0 (MicroRNAs)
RN  - 3768-18-1 (N-acetylcytidine)
RN  - 0 (RNA, Messenger)
RN  - 0 (FOXM1 protein, human)
RN  - 0 (Forkhead Box Protein M1)
RN  - EC 2.3.1.88 (NAT10 protein, human)
RN  - EC 2.3.1.88 (N-Terminal Acetyltransferases)
SB  - IM
MH  - Animals
MH  - Humans
MH  - Squamous Cell Carcinoma of Head and Neck/genetics
MH  - *MicroRNAs/genetics
MH  - RNA, Messenger/genetics
MH  - *Laryngeal Neoplasms/metabolism
MH  - Cell Line, Tumor
MH  - *Head and Neck Neoplasms
MH  - Carcinogenesis/genetics
MH  - Cell Transformation, Neoplastic
MH  - Forkhead Box Protein M1/genetics
MH  - N-Terminal Acetyltransferases
PMC - PMC10898813
OTO - NOTNLM
OT  - FOXM1
OT  - LSCC
OT  - NAT10
OT  - ac4C
OT  - migration
OT  - proliferation
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2023/11/10 18:43
MHDA- 2023/11/13 06:42
PMCR- 2023/11/10
CRDT- 2023/11/10 12:13
PHST- 2023/11/13 06:42 [medline]
PHST- 2023/11/10 18:43 [pubmed]
PHST- 2023/11/10 12:13 [entrez]
PHST- 2023/11/10 00:00 [pmc-release]
AID - 2274143 [pii]
AID - 10.1080/15384047.2023.2274143 [doi]
PST - ppublish
SO  - Cancer Biol Ther. 2023 Dec 31;24(1):2274143. doi: 10.1080/15384047.2023.2274143. 
      Epub 2023 Nov 10.