PMID- 20512084
OWN - NLM
STAT- MEDLINE
DCOM- 20100928
LR  - 20181201
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Linking)
VI  - 16
IP  - 6
DP  - 2010 Jun
TI  - SH3GL2 gene participates in MEK-ERK signal pathway partly by regulating EGFR in 
      the laryngeal carcinoma cell line Hep2.
PG  - BR168-73
AB  - BACKGROUND: The human Src homology 3 (SH3) domain GRB2-like 2 (SH3GL2) gene, a 
      novel tumor suppressor gene in laryngeal squamous cell carcinoma (LSCC), induces 
      apoptosis of tumor cells by regulating intra-cellular signal transduction 
      networks. The objective of this study was to investigate the molecular mechanism 
      of SH3GL2 in laryngeal carcinogenesis. MATERIAL/METHODS: RNA interference 
      inhibited the expression of level of SH3GL, and RT-PCR and Western blotting were 
      applied to evaluate the expression level of SH3GL2 after RNA interference. After 
      RNA interference, flow cytometry and 3-(4,5-dimethyl-2-thiazolyl)-2, 
      5-diphenyl-2H-tetrazolium bromide (MTT) assay were used to detect the biological 
      effects, and Western blotting was used to determine the expression of EGFR and 
      phosphorylated ERK1/2. The Hep2 cells transfected with siRNA-SH3GL2 were treated 
      by U0126 (selective MEK1/2 Inhibitor), and the phosphorylated ERK1/2 proteins 
      were detected by Western blotting; cell proliferation and apoptosis were detected 
      subsequently. RESULTS: Our results show that the expression level of epidermal 
      growth factor receptor (EGFR) and phosphorylated extracellular signal-regulated 
      kinase 1/2 (ERK1/2) were up-regulated after down-regulation of SH3GL2. 
      Additionally, SH3GL2 promoted apoptosis while decreasing cell proliferation. 
      However, if ERK1/2 was inhibited by U0126, the apoptosis rate increased and 
      proliferation decreased inversely. CONCLUSIONS: SH3GL2 participates in the 
      regulation of apoptosis through the MEK-ERK signal pathway by adjusting EGFR in 
      the laryngeal carcinoma cell line Hep2.
FAU - Shang, Chao
AU  - Shang C
AD  - Department of Neurobiology, China Medical University, Shenyang, PR China.
FAU - Guo, Yan
AU  - Guo Y
FAU - Fu, Shuang
AU  - Fu S
FAU - Fu, Weineng
AU  - Fu W
FAU - Sun, Kailai
AU  - Sun K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (DNA Primers)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (SH3GL2 protein, human)
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/*genetics/*physiology
MH  - Apoptosis
MH  - Cell Line, Tumor
MH  - DNA Primers/genetics
MH  - ErbB Receptors/*metabolism
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Laryngeal Neoplasms/*diagnosis
MH  - Mitogen-Activated Protein Kinase 3/*metabolism
MH  - Mitogen-Activated Protein Kinase Kinases/*metabolism
MH  - Models, Biological
MH  - Phosphorylation
MH  - RNA, Small Interfering/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction
EDAT- 2010/06/01 06:00
MHDA- 2010/09/30 06:00
CRDT- 2010/06/01 06:00
PHST- 2010/06/01 06:00 [entrez]
PHST- 2010/06/01 06:00 [pubmed]
PHST- 2010/09/30 06:00 [medline]
AID - 880604 [pii]
PST - ppublish
SO  - Med Sci Monit. 2010 Jun;16(6):BR168-73.