PMID- 37757768
OWN - NLM
STAT- Publisher
LR  - 20230927
IS  - 1421-9859 (Electronic)
IS  - 0378-5866 (Linking)
DP  - 2023 Sep 27
TI  - ABCF1/CXCL12/CXCR4 Enhances Glioblastoma Cell Proliferation, Migration, and 
      Invasion by Activating the PI3K/AKT Signal Pathway.
PG  - 1-10
LID - 10.1159/000533130 [doi]
AB  - Glioblastoma (GBM) is the most prevalent and fatal form of brain tumor, which is 
      associated with a poor prognosis. ATP-binding cassette subfamily F member 1 
      (ABCF1) is an E2 ubiquitin-conjugating enzyme, which is implicated in regulating 
      immune responses and tumorigenesis. Aberrant E3 ubiquitylation has been evidenced 
      in GBM. However, the role of ABCF1 in GBM needs to be further explored. The 
      expression of ABCF1, CXC chemokine ligand 12 (CXCL12), and CXC chemokine receptor 
      4 (CXCR4) in GBM tissues was examined by the GEPIA tool, real-time PCR and 
      Western blotting. HMC3, U251MG, and LN-229 cells were cultured and transfected 
      with shRNA targeting ABCF1 and ABCF1 plasmids. The proliferative, migrative, and 
      invasive ability of cells was detected. Western blotting was used to detect the 
      levels of phosphorylated phosphatidylinositol 3-kinase (PI3K) and phosphorylated 
      protein kinase B (AKT). We observed that GBM tissues had higher ABCF1, CXCL12, 
      and CXCR4 expression levels. The expression levels of CXCL12 and CXCR4 were 
      enhanced by ABCF1 overexpression, which were significantly reversed by silence of 
      ABCF1 in GBM cells. Silencing ABCF1 or CXCR4 inhibition weakened the capacity of 
      GBM cell growth, migration, and invasion, while ectopic ABCF1 expression or 
      CXCL12 treatment enhanced the cellular function of GBM cells. Furthermore, p-PI3K 
      and p-AKT protein levels were downregulated by ABCF1 knockdown or CXCR4 blockade, 
      which were prompted by ABCF1 overexpression or CXCL12 supplement. The 
      ABCF1-CXCL12-CXCR4 axis was identified as a key player in GBM cell survival and 
      metastasis by activating the PI3K/AKT signaling pathway in GBM cells.
CI  - (c) 2023 The Author(s). Published by S. Karger AG, Basel.
FAU - Yin, Xiaohong
AU  - Yin X
AD  - Department of Neurosurgery, Guangyuan Central Hospital, Guangyuan, China.
FAU - Xia, Keshun
AU  - Xia K
AD  - Department of Neurosurgery, Guangyuan Central Hospital, Guangyuan, China.
FAU - Peng, Song
AU  - Peng S
AD  - Department of Neurosurgery, Guangyuan Central Hospital, Guangyuan, China.
FAU - Tan, Bo
AU  - Tan B
AD  - Department of Neurosurgery, Guangyuan Central Hospital, Guangyuan, China.
FAU - Huang, Yaohui
AU  - Huang Y
AD  - Department of Neurosurgery, Guangyuan Central Hospital, Guangyuan, China.
FAU - Wang, Mao
AU  - Wang M
AD  - Department of Neurosurgery, Guangyuan Central Hospital, Guangyuan, China.
FAU - He, Mingfang
AU  - He M
AD  - Department of Neurosurgery, Guangyuan Central Hospital, Guangyuan, China.
LA  - eng
PT  - Journal Article
DEP - 20230927
PL  - Switzerland
TA  - Dev Neurosci
JT  - Developmental neuroscience
JID - 7809375
SB  - IM
OTO - NOTNLM
OT  - ABCF1
OT  - CXCL12
OT  - CXCR4
OT  - Glioblastoma
OT  - PI3K/AKT signal pathway
EDAT- 2023/09/28 00:42
MHDA- 2023/09/28 00:42
CRDT- 2023/09/27 18:23
PHST- 2022/12/26 00:00 [received]
PHST- 2023/07/03 00:00 [accepted]
PHST- 2023/09/28 00:42 [medline]
PHST- 2023/09/28 00:42 [pubmed]
PHST- 2023/09/27 18:23 [entrez]
AID - 000533130 [pii]
AID - 10.1159/000533130 [doi]
PST - aheadofprint
SO  - Dev Neurosci. 2023 Sep 27:1-10. doi: 10.1159/000533130.