PMID- 25636507
OWN - NLM
STAT- MEDLINE
DCOM- 20160425
LR  - 20220311
IS  - 1559-131X (Electronic)
IS  - 1357-0560 (Linking)
VI  - 32
IP  - 3
DP  - 2015 Mar
TI  - GPCR48/LGR4 promotes tumorigenesis of prostate cancer via PI3K/Akt signaling 
      pathway.
PG  - 49
LID - 10.1007/s12032-015-0486-1 [doi]
AB  - G-protein-coupled receptor (GPCR) 48, also known as leucine-rich 
      repeat-containing G-protein-coupled receptor (LGR) 4, is an orphan receptor 
      belonging to the GPCR superfamily, which plays an important role in the 
      development of various organs and multiple cancers. However, the function of 
      GPCR48/LGR4 in prostate cancer has not been fully investigated. Herein, 
      GPCR48/LGR4 was overexpressed and silenced in prostate cancer cells via plasmid 
      and shRNA transfection, respectively. The expression of GPCR48/LGR4 in mRNA and 
      protein levels was analyzed using RT-qPCR and Western blotting, respectively. 
      Subsequently, we demonstrated the effects of GPCR48/LGR4 on the migration, 
      invasion, proliferation and apoptosis of prostate cancer cells, including Du145 
      and PC-3 cells. Next, we investigated the relationship between GPCR48/LGR4 and 
      phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt signaling pathway. The 
      results showed that the overexpression of GPCR48/LGR4 was associated with the 
      up-regulation of Akt, a key effector of PI3K/Akt signaling pathway, which 
      meantime up-regulated the expression of mammalian target of rapamycin (mTOR) and 
      glycogen synthase kinase 3beta (GSK-3beta), while down-regulated forkhead box, class O 
      (FOXO), all of whom are the downstream targets of PI3K/Akt signaling pathway. 
      Hence, the results suggested that GPCR48/LGR4 may regulate prostate cancer cells 
      and tumor growth via the PI3K/Akt signaling pathway and could provide a better 
      therapeutic target for the diagnosis and treatment of prostate cancer.
FAU - Liang, Fang
AU  - Liang F
AD  - Department of Oncology, Zhengzhou Central Hospital Affiliated to Zhengzhou 
      University, Zhengzhou, China.
FAU - Yue, Junmin
AU  - Yue J
FAU - Wang, Junyong
AU  - Wang J
FAU - Zhang, Lijuan
AU  - Zhang L
FAU - Fan, Rui
AU  - Fan R
FAU - Zhang, Hao
AU  - Zhang H
FAU - Zhang, Qingsong
AU  - Zhang Q
LA  - eng
PT  - Journal Article
DEP - 20150131
PL  - United States
TA  - Med Oncol
JT  - Medical oncology (Northwood, London, England)
JID - 9435512
RN  - 0 (LGR4 protein, human)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (GSK3B protein, human)
RN  - EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
RN  - EC 2.7.11.1 (Gsk3b protein, mouse)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.26 (Glycogen Synthase Kinase 3)
SB  - IM
MH  - Animals
MH  - Apoptosis/genetics
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics
MH  - Cell Proliferation/genetics
MH  - Gene Expression Regulation, Neoplastic
MH  - Glycogen Synthase Kinase 3/genetics/metabolism
MH  - Glycogen Synthase Kinase 3 beta
MH  - Humans
MH  - Male
MH  - Mice, Nude
MH  - Phosphatidylinositol 3-Kinases/*metabolism
MH  - Prostatic Neoplasms/genetics/metabolism/*pathology
MH  - Proto-Oncogene Proteins c-akt/genetics/*metabolism
MH  - Receptors, G-Protein-Coupled/genetics/*metabolism
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/genetics/metabolism
MH  - Xenograft Model Antitumor Assays
EDAT- 2015/02/01 06:00
MHDA- 2016/04/26 06:00
CRDT- 2015/02/01 06:00
PHST- 2014/12/22 00:00 [received]
PHST- 2015/01/22 00:00 [accepted]
PHST- 2015/02/01 06:00 [entrez]
PHST- 2015/02/01 06:00 [pubmed]
PHST- 2016/04/26 06:00 [medline]
AID - 10.1007/s12032-015-0486-1 [doi]
PST - ppublish
SO  - Med Oncol. 2015 Mar;32(3):49. doi: 10.1007/s12032-015-0486-1. Epub 2015 Jan 31.