PMID- 31002126
OWN - NLM
STAT- MEDLINE
DCOM- 20200813
LR  - 20211204
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 7
DP  - 2019 Apr
TI  - SGK2 promotes renal cancer progression via enhancing ERK 1/2 and AKT 
      phosphorylation.
PG  - 2756-2767
LID - 17549 [pii]
LID - 10.26355/eurrev_201904_17549 [doi]
AB  - OBJECTIVE: Increasing studies reported that the serum- and 
      glucocorticoid-inducible kinases (SGKs) contributed to the tumorigenesis of 
      various cancer. In this article, we are aiming to explore the function of SGK2 in 
      renal cell cancer (RCC). PATIENTS AND METHODS: In this study, the SGK2 expression 
      was quantified by Western blot (WB) in multiple RCC cell lines. And in vitro SGK2 
      knockdown and overexpression experiments were also performed. In addition, 
      molecular function analysis was performed using FunRich software V3. The Cancer 
      Genome Atlas (TCGA) database was retrieved to verify the association between the 
      SGK2 expression and the prognosis of RCC patients. RESULTS: We found that SGK2 
      was up-regulated in RCC tissues compared with adjacent normal tissues, and the 
      SGK2 expression also increased in various RCC cell lines compared to that in the 
      normal epithelial cell line HK-2. Meanwhile, the SGK2 expression was 
      significantly associated with the survival rate of RCC patients. Functional 
      experiments showed that silencing SGK2 expression inhibited RCC cells 
      proliferation, migration, colony formation and invasion abilities in vitro, 
      whereas opposite results were uncovered after overexpressing SGK2 in RCC cells. 
      Furthermore, functional analyses showed that SGK2 related genes were associated 
      with protein serine/threonine kinase activity, guanosine triphosphatase (GTPase) 
      activity, guanyl-nucleotide exchange factor activity, and motor activity. Protein 
      interaction analysis identified that growth factor receptor-bound protein 2 
      (GRB2), one of the most important upstream components in the growth factor 
      signaling pathway, was significantly enriched in SGK2 related genes. In addition, 
      the WB assay validated that SGK2 could promote the phosphorylation of ERK 1/2 and 
      AKT. CONCLUSIONS: Our results suggested that SGK2 promoted RCC progression by 
      mediating the phosphorylation of extracellular regulated protein kinases (ERK) 
      1/2 and Protein kinase B (AKT/PKB), indicating that SGK2 might serve as a 
      potential prognostic marker and therapeutic target for renal cancer patients.
FAU - Liu, Y
AU  - Liu Y
AD  - Department of Urology, the First Affiliated Hospital of Anhui Medical University, 
      Hefei, Anhui, China. liang_chaozhao@ahmu.edu.cn.
FAU - Chen, J-B
AU  - Chen JB
FAU - Zhang, M
AU  - Zhang M
FAU - Zhang, X-L
AU  - Zhang XL
FAU - Meng, J-L
AU  - Meng JL
FAU - Zhou, J
AU  - Zhou J
FAU - Hao, Z-Y
AU  - Hao ZY
FAU - Zhang, L
AU  - Zhang L
FAU - Zu, X-B
AU  - Zu XB
FAU - Liang, C-Z
AU  - Liang CZ
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Immediate-Early Proteins)
RN  - 86-01-1 (Guanosine Triphosphate)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (serum-glucocorticoid regulated kinase)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Carcinoma, Renal Cell/*metabolism
MH  - Cell Line, Tumor/metabolism
MH  - Disease Progression
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Female
MH  - Guanosine Triphosphate/metabolism
MH  - Humans
MH  - Immediate-Early Proteins/*metabolism
MH  - Kidney Neoplasms/*pathology
MH  - MAP Kinase Signaling System
MH  - Male
MH  - Phosphorylation
MH  - Protein Serine-Threonine Kinases/*metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - *Up-Regulation
EDAT- 2019/04/20 06:00
MHDA- 2020/08/14 06:00
CRDT- 2019/04/20 06:00
PHST- 2019/04/20 06:00 [entrez]
PHST- 2019/04/20 06:00 [pubmed]
PHST- 2020/08/14 06:00 [medline]
AID - 17549 [pii]
AID - 10.26355/eurrev_201904_17549 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Apr;23(7):2756-2767. doi: 
      10.26355/eurrev_201904_17549.