Expressions of ezrin, ERK, STAT3, and AKT in tongue cancer and association with tumor characteristics and patient survival.
Adult
Aged
Aged, 80 and over
Biomarkers, Tumor
/ metabolism
Carcinoma, Squamous Cell
/ metabolism
Cytoskeletal Proteins
/ metabolism
Female
Follow-Up Studies
Humans
Male
Middle Aged
Mitogen-Activated Protein Kinase 1
/ metabolism
Mitogen-Activated Protein Kinase 3
/ metabolism
Prognosis
Proto-Oncogene Proteins c-akt
/ metabolism
STAT3 Transcription Factor
/ metabolism
Survival Rate
Tongue Neoplasms
/ metabolism
AKT
ERK
the 5-year survival rate
tongue squamous cell carcinoma
Journal
Clinical and experimental dental research
ISSN: 2057-4347
Titre abrégé: Clin Exp Dent Res
Pays: United States
ID NLM: 101692332
Informations de publication
Date de publication:
08 2020
08 2020
Historique:
received:
21
10
2019
revised:
07
02
2020
accepted:
06
03
2020
pubmed:
14
4
2020
medline:
24
8
2021
entrez:
14
4
2020
Statut:
ppublish
Résumé
Ezrin, ERK, STAT3, and AKT are proteins that are overexpressed in various types of cancer, although their expressions in tongue cancer has received less focus. This study aimed to address associations between the expression levels of these proteins and with characteristics of the tumor and patient survival. We performed immunohistochemical staining of ezrin, ERK, STAT3, and AKT in tumors from patients with tongue carcinoma in situ (CIS, n = 17) and tongue squamous cell carcinoma (SCC, n = 46). Statistical differences between the SCC versus the CIS cohorts were estimated by calculations of bivariate odds ratios of low versus high expression of the proteins. Fisher's exact tests were used to appraise interassociations between the proteins, as well as expression levels versus patient and tumor characteristics. Survival based on Kaplan-Meier statistics in combination log-rank tests were used to address potential effects of the patient and tumor characteristics versus 5-year survival rate. The relative high: low expression of all four proteins in the two cohorts differed, and particularly ERK was markedly overexpressed in the SCC versus the CIS cohort (odds ratio = 45.3, p < .01). The relative high: low expression each protein versus patient and tumor characteristics; showed associations between AKT expression and T stage (p = .002) plus node metastases (p = .12), and between ERK expression and drinking (p = .01) and smoking history (p = .01). There was no significant difference observed between ERK and the three other molecules, nor any significant difference between the degree of expression of each protein and the 5-year disease-specific survival rate. Ezrin, ERK, STAT3, and AKT appear to be involved in the progress from carcinoma in situ in the tongue into squamous cell carcinoma. ERK in particular is overexpressed, suggesting that ERK may be a novel therapeutic target for preventing tongue cancer.
Sections du résumé
BACKGROUND
Ezrin, ERK, STAT3, and AKT are proteins that are overexpressed in various types of cancer, although their expressions in tongue cancer has received less focus. This study aimed to address associations between the expression levels of these proteins and with characteristics of the tumor and patient survival.
METHODS
We performed immunohistochemical staining of ezrin, ERK, STAT3, and AKT in tumors from patients with tongue carcinoma in situ (CIS, n = 17) and tongue squamous cell carcinoma (SCC, n = 46). Statistical differences between the SCC versus the CIS cohorts were estimated by calculations of bivariate odds ratios of low versus high expression of the proteins. Fisher's exact tests were used to appraise interassociations between the proteins, as well as expression levels versus patient and tumor characteristics. Survival based on Kaplan-Meier statistics in combination log-rank tests were used to address potential effects of the patient and tumor characteristics versus 5-year survival rate.
RESULTS
The relative high: low expression of all four proteins in the two cohorts differed, and particularly ERK was markedly overexpressed in the SCC versus the CIS cohort (odds ratio = 45.3, p < .01). The relative high: low expression each protein versus patient and tumor characteristics; showed associations between AKT expression and T stage (p = .002) plus node metastases (p = .12), and between ERK expression and drinking (p = .01) and smoking history (p = .01). There was no significant difference observed between ERK and the three other molecules, nor any significant difference between the degree of expression of each protein and the 5-year disease-specific survival rate.
CONCLUSION
Ezrin, ERK, STAT3, and AKT appear to be involved in the progress from carcinoma in situ in the tongue into squamous cell carcinoma. ERK in particular is overexpressed, suggesting that ERK may be a novel therapeutic target for preventing tongue cancer.
Identifiants
pubmed: 32281236
doi: 10.1002/cre2.293
pmc: PMC7453773
doi:
Substances chimiques
Biomarkers, Tumor
0
Cytoskeletal Proteins
0
STAT3 Transcription Factor
0
STAT3 protein, human
0
ezrin
0
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
MAPK1 protein, human
EC 2.7.11.24
MAPK3 protein, human
EC 2.7.11.24
Mitogen-Activated Protein Kinase 1
EC 2.7.11.24
Mitogen-Activated Protein Kinase 3
EC 2.7.11.24
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
420-427Informations de copyright
© 2020 The Authors. Clinical and Experimental Dental Research published by John Wiley & Sons Ltd.
Références
Int J Gynecol Pathol. 2006 Apr;25(2):121-30
pubmed: 16633060
Cancer Lett. 1999 Dec 1;147(1-2):31-8
pubmed: 10660086
Carcinogenesis. 2013 Nov;34(11):2673-81
pubmed: 23784083
PLoS One. 2013;8(1):e54881
pubmed: 23357878
Science. 1999 Nov 26;286(5445):1741-4
pubmed: 10576742
PLoS One. 2013 May 17;8(5):e62823
pubmed: 23690956
Int J Cancer. 2009 Jun 1;124(11):2549-58
pubmed: 19165868
Zhonghua Nan Ke Xue. 2017 May;23(5):406-411
pubmed: 29717829
Oncol Lett. 2018 Apr;15(4):4278-4288
pubmed: 29541195
Mod Pathol. 2005 Apr;18(4):503-10
pubmed: 15475929
Clin Exp Dent Res. 2020 Aug;6(4):420-427
pubmed: 32281236
Nat Med. 2004 Feb;10(2):182-6
pubmed: 14704791
Int J Cancer. 2003 May 1;104(5):527-32
pubmed: 12594806
Cancer Biol Ther. 2014 Mar 1;15(3):245-6
pubmed: 24424114
Clin Cancer Res. 2004 Jun 15;10(12 Pt 1):4029-37
pubmed: 15217935
Oral Oncol. 2007 Oct;43(9):894-7
pubmed: 17307026
Oncogene. 2007 May 14;26(22):3291-310
pubmed: 17496923
Cell Biochem Funct. 2012 Jun;30(4):340-6
pubmed: 22302289
Cancer. 2005 Dec 1;104(11):2430-6
pubmed: 16245318
Clin Cancer Res. 2005 Sep 1;11(17):6198-204
pubmed: 16144921
J Dig Dis. 2009 Nov;10(4):258-64
pubmed: 19906104
Clin Cancer Res. 2013 Nov 1;19(21):5940-51
pubmed: 23918606
Int J Oral Sci. 2018 Oct 22;10(4):30
pubmed: 30344309
Neoplasia. 2016 Feb;18(2):111-20
pubmed: 26936397
Cancer Lett. 2013 Sep 1;337(2):293-300
pubmed: 23587796
Tumour Biol. 2014 Jul;35(7):6455-65
pubmed: 24682903
Am J Pathol. 2012 Jun;180(6):2462-78
pubmed: 22546478
Oncol Lett. 2017 Sep;14(3):2859-2863
pubmed: 28927043
Cancer. 2012 Jan 1;118(1):101-11
pubmed: 21717431
Oral Oncol. 2004 Feb;40(2):110-9
pubmed: 14693233