PMID- 28090628
OWN - NLM
STAT- MEDLINE
DCOM- 20180515
LR  - 20180515
IS  - 1699-5848 (Electronic)
IS  - 0213-3911 (Linking)
VI  - 32
IP  - 10
DP  - 2017 Oct
TI  - ERK1/2, JNK and STAT3 activation and correlation with tumor differentiation in 
      oral SCC.
PG  - 1065-1076
LID - 10.14670/HH-11-868 [doi]
AB  - Signal transducer and activator of transcription 3 (STAT3) and mitogen activated 
      protein kinases (MAPKs), including ERK and JNK, have been implicated in oral 
      squamous cell carcinoma (OSCC) development and progression. Our purpose was to 
      evaluate the levels of activated STAT3, ERK1/2 and JNK by immunohistochemistry in 
      OSCC and to investigate possible correlations of these molecules with each other 
      as well as with the degree of tumor differentiation. Immunohistochemical 
      assessment of the phosphorylated levels of STAT3(tyrosine/ serine), ERK1/2 and 
      JNK was performed in 60 OSCC, including well, moderately and poorly 
      differentiated tumors. Semiquantitative scoring system was used, by calculating 
      intensity of immunostaining, percentage of positive cells and combined scores. 
      Statistics included Fisher's test, Student's T-Test and Kruskal-Wallis analysis, 
      Spearman's correlation coefficient and multivariate logistic regression analyses. 
      Immunohistochemical levels of both pSTAT3(tyr) and pERK1/2 showed statistically 
      significant differences between well and poorly differentiated tumors with the 
      latter receiving higher mean percentage, intensity and total scores. On the other 
      hand, pJNK showed statistically significantly higher intensity levels in 
      moderately compared to poorly differentiated tumors. pSTAT3(ser) immunoexpression 
      did not appear to correlate with tumor differentiation. Between different 
      molecules, more pronounced, pERK1/2 levels exhibited statistically significant 
      positive correlation with pSTAT3(ser), pSTAT3(tyr) and pJNK expression. ERK1/2 
      and STAT3 activation (as assessed by tyrosine but not serine phosphorylation) 
      could contribute to a less differentiated phenotype in OSCC, while JNK activation 
      may have an opposite, although possibly less pronounced, effect. Positive 
      correlations between MAPK and STAT3 levels may indicate a direct crosstalk and/or 
      regulation by common upstream pathways.
FAU - Gkouveris, I
AU  - Gkouveris I
AD  - Department of Oral Pathology and Medicine, Dental School, National and 
      Kapodistrian University of Athens, Athens, Greece. igkouver@gmail.com.
FAU - Nikitakis, N
AU  - Nikitakis N
AD  - Department of Oral Pathology and Medicine, Dental School, National and 
      Kapodistrian University of Athens, Athens, Greece.
FAU - Avgoustidis, D
AU  - Avgoustidis D
AD  - Department of Oral and Maxillofacial Surgery, "Evaggelismos" Hospital, National 
      and Kapodistrian University of Athens, Athens, Greece.
FAU - Karanikou, M
AU  - Karanikou M
AD  - First Department of Pathology, Medical School, National and Kapodistrian 
      University of Athens, Athens, Greece.
FAU - Rassidakis, G
AU  - Rassidakis G
AD  - First Department of Pathology, Medical School, National and Kapodistrian 
      University of Athens, Athens, Greece.
FAU - Sklavounou, A
AU  - Sklavounou A
AD  - Department of Oral Pathology and Medicine, Dental School National and 
      Kapodistrian University of Athens, Athens, Greece.
LA  - eng
PT  - Journal Article
DEP - 20170116
PL  - Spain
TA  - Histol Histopathol
JT  - Histology and histopathology
JID - 8609357
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
RN  - 42HK56048U (Tyrosine)
RN  - 452VLY9402 (Serine)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Carcinoma, Squamous Cell/*genetics/metabolism/*pathology
MH  - Cell Differentiation
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - MAP Kinase Signaling System/*genetics
MH  - Male
MH  - Middle Aged
MH  - Mitogen-Activated Protein Kinases/*biosynthesis/genetics
MH  - Mouth Neoplasms/*genetics/metabolism/*pathology
MH  - Neoplasm Grading
MH  - Phosphorylation
MH  - STAT3 Transcription Factor/*biosynthesis/genetics
MH  - Serine/metabolism
MH  - Tyrosine/metabolism
EDAT- 2017/01/17 06:00
MHDA- 2018/05/16 06:00
CRDT- 2017/01/17 06:00
PHST- 2017/01/17 06:00 [pubmed]
PHST- 2018/05/16 06:00 [medline]
PHST- 2017/01/17 06:00 [entrez]
AID - HH-11-868 [pii]
AID - 10.14670/HH-11-868 [doi]
PST - ppublish
SO  - Histol Histopathol. 2017 Oct;32(10):1065-1076. doi: 10.14670/HH-11-868. Epub 2017 
      Jan 16.