PMID- 35333690
OWN - NLM
STAT- MEDLINE
DCOM- 20220426
LR  - 20220716
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 4
DP  - 2022 Apr
TI  - Cullin 4A/protein arginine methyltransferase 5 (CUL4A/PRMT5) promotes cell 
      malignant phenotypes and tumor growth in nasopharyngeal carcinoma.
PG  - 8712-8723
LID - 10.1080/21655979.2022.2054756 [doi]
AB  - Targeted therapy is an important therapeutic strategy currently, however, the 
      development of targeted therapy for nasopharyngeal carcinoma (NPC) is relatively 
      lagging. Cullin 4A (CUL4A) was reported to be overexpressed in NPC; nevertheless, 
      the specific role of CUL4A remains unrevealed. NPC cells and tumor-bearing mice 
      were cultivated to explore the role and mechanism of CUL4A in NPC. After 
      evaluating CUL4A levels in NPC cells, functional experiments were carried out to 
      investigate the effects of CUL4A knockdown and overexpression on cell 
      proliferative, invasive and migratory aptitude as well as NF-kappaB signaling. 
      Following the GeneMANIA database predicted that protein arginine 
      methyltransferase 5 (PRMT5) was downstream of CUL4A, the mediated role of PRMT5 
      in the regulation of CUL4A on cells was then determined. Moreover, the tumor 
      volumes and weights of tumor-bearing mice were recorded, and the levels of 
      proliferation-, migration-, and NF-kappaB signaling-related proteins in the tumor 
      were determined. Herein, CUL4A was enhanced in NPC cells, and its knockdown and 
      overexpression separately suppressed and promoted cell proliferative, invasive, 
      and migratory aptitude as well as NF-kappaB signal activation. Novelty, PRMT5 
      knockdown reversed the influences of CUL4A overexpression on these aspects. In 
      addition, its knockdown likewise reversed the facilitating impact of CUL4A 
      expression on tumor growth and declined the expression levels of proliferation-, 
      migration-, and NF-kappaB signaling-related protein in the tumor. Together, this 
      paper indicated that CUL4A promoted the proliferative, invasive, and migratory 
      aptitude of NPC cells as well as tumor growth by promoting PRMT5 to activate 
      NF-kappaB signaling.
FAU - Sun, Xiuying
AU  - Sun X
AD  - Department of Otolaryngology, The Affiliated Huai'an No. 1 People's Hospital of 
      Nanjing Medical University, Huai'an, Jiangsu, China.
FAU - Zhou, Jinhui
AU  - Zhou J
AD  - Department of Otolaryngology, The Affiliated Huai'an No. 1 People's Hospital of 
      Nanjing Medical University, Huai'an, Jiangsu, China.
FAU - Zhang, Zhicun
AU  - Zhang Z
AD  - Department of Otolaryngology, The Affiliated Huai'an No. 1 People's Hospital of 
      Nanjing Medical University, Huai'an, Jiangsu, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (Cul4a protein, mouse)
RN  - 0 (Cullin Proteins)
RN  - 0 (NF-kappa B)
RN  - EC 2.1.1.319 (Prmt5 protein, mouse)
RN  - EC 2.1.1.319 (Protein-Arginine N-Methyltransferases)
SB  - IM
MH  - Animals
MH  - Cell Line, Tumor
MH  - Cell Proliferation/genetics
MH  - *Cullin Proteins/genetics/metabolism
MH  - Mice
MH  - NF-kappa B/genetics/metabolism
MH  - Nasopharyngeal Carcinoma/genetics
MH  - *Nasopharyngeal Neoplasms/metabolism
MH  - Phenotype
MH  - *Protein-Arginine N-Methyltransferases/genetics/metabolism
PMC - PMC9161857
OTO - NOTNLM
OT  - C666-1 cell
OT  - Cullin 4A
OT  - nasopharyngeal carcinoma
OT  - p65
OT  - protein arginine methyltransferase 5
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2022/03/26 06:00
MHDA- 2022/04/27 06:00
PMCR- 2022/03/25
CRDT- 2022/03/25 17:18
PHST- 2022/03/25 17:18 [entrez]
PHST- 2022/03/26 06:00 [pubmed]
PHST- 2022/04/27 06:00 [medline]
PHST- 2022/03/25 00:00 [pmc-release]
AID - 2054756 [pii]
AID - 10.1080/21655979.2022.2054756 [doi]
PST - ppublish
SO  - Bioengineered. 2022 Apr;13(4):8712-8723. doi: 10.1080/21655979.2022.2054756.