S6 ribosomal protein phosphorylation is associated with malignancy of intraductal papillary mucinous neoplasm of the pancreas.
18F‐Ffluorodeoxyglucose positron emission tomography
glucose transporter 1
intraductal papillary mucinous neoplasms
mammalian target of rapamycin complex 1
phosphorylated S6 ribosomal protein
Journal
Annals of gastroenterological surgery
ISSN: 2475-0328
Titre abrégé: Ann Gastroenterol Surg
Pays: Japan
ID NLM: 101718062
Informations de publication
Date de publication:
Sep 2020
Sep 2020
Historique:
received:
12
05
2020
revised:
25
05
2020
accepted:
27
05
2020
entrez:
2
10
2020
pubmed:
3
10
2020
medline:
3
10
2020
Statut:
epublish
Résumé
Glucose metabolism of intraductal papillary mucinous neoplasms (IPMNs) of the pancreas is unclear. S6 ribosomal protein (S6) phosphorylation is involved not only in controlling cell growth but also in glucose metabolism in cancer. The aim of this study was to investigate the role of S6 phosphorylation and the significance of glucose metabolic changes in IPMN. Records of 39 patients who underwent preoperative FDG-PET and curative resection were enrolled in this study. S6 phosphorylation and GLUT1 expression were evaluated immunohistochemically in these patients. The effect of S6 phosphorylation on glucose uptake was examined in cancer cell lines. To examine the change of glucose metabolism in IPMN clinically, the relation between clinical factors including FDG-PET and malignancy of IPMN was investigated. S6 phosphorylation and GLUT1 expression were significantly higher in carcinoma than in normal cells or adenoma. Cell lines with high level of S6 phosphorylation showed high glucose uptake, and inhibition of S6 phosphorylation reduced glucose uptake. In clinical examination, FDG-PET was the independent factor related to the diagnosis of adenoma or carcinoma (odds ratio = 20.0, 95% confidence interval = 1.837-539.9, S6 phosphorylation was associated with glucose uptake and malignancy of IPMN. Moreover, glucose uptake increased in malignant cells of IPMN, and FDG-PET is useful for detecting malignancy of IPMN.
Sections du résumé
BACKGROUND
BACKGROUND
Glucose metabolism of intraductal papillary mucinous neoplasms (IPMNs) of the pancreas is unclear. S6 ribosomal protein (S6) phosphorylation is involved not only in controlling cell growth but also in glucose metabolism in cancer. The aim of this study was to investigate the role of S6 phosphorylation and the significance of glucose metabolic changes in IPMN.
METHODS
METHODS
Records of 39 patients who underwent preoperative FDG-PET and curative resection were enrolled in this study. S6 phosphorylation and GLUT1 expression were evaluated immunohistochemically in these patients. The effect of S6 phosphorylation on glucose uptake was examined in cancer cell lines. To examine the change of glucose metabolism in IPMN clinically, the relation between clinical factors including FDG-PET and malignancy of IPMN was investigated.
RESULTS
RESULTS
S6 phosphorylation and GLUT1 expression were significantly higher in carcinoma than in normal cells or adenoma. Cell lines with high level of S6 phosphorylation showed high glucose uptake, and inhibition of S6 phosphorylation reduced glucose uptake. In clinical examination, FDG-PET was the independent factor related to the diagnosis of adenoma or carcinoma (odds ratio = 20.0, 95% confidence interval = 1.837-539.9,
CONCLUSION
CONCLUSIONS
S6 phosphorylation was associated with glucose uptake and malignancy of IPMN. Moreover, glucose uptake increased in malignant cells of IPMN, and FDG-PET is useful for detecting malignancy of IPMN.
Identifiants
pubmed: 33005852
doi: 10.1002/ags3.12367
pii: AGS312367
pmc: PMC7511561
doi:
Types de publication
Journal Article
Langues
eng
Pagination
571-579Informations de copyright
© 2020 The Authors. Annals of Gastroenterological Surgery published by John Wiley & Sons Australia, Ltd on behalf of The Japanese Society of Gastroenterological Surgery.
Déclaration de conflit d'intérêts
Conflict of interest: The authors declare no conflict of interests related to this article.
Références
Pancreatology. 2017 Sep - Oct;17(5):738-753
pubmed: 28735806
Metabolism. 2016 Feb;65(2):124-39
pubmed: 26773935
Invest New Drugs. 2014 Jun;32(3):510-7
pubmed: 24395457
PLoS One. 2014 Feb 03;9(2):e87875
pubmed: 24498386
Lung Cancer. 2014 Feb;83(2):197-204
pubmed: 24365102
Nat Rev Cancer. 2011 Feb;11(2):85-95
pubmed: 21258394
Pancreatology. 2012 May-Jun;12(3):183-97
pubmed: 22687371
Front Cell Dev Biol. 2018 Sep 25;6:122
pubmed: 30320109
J Nucl Med. 1997 Sep;38(9):1337-44
pubmed: 9293783
Pancreatology. 2017 Nov - Dec;17(6):920-926
pubmed: 28890154
Cancer. 1998 Jul 1;83(1):34-40
pubmed: 9655290
Ann Nucl Med. 2011 Aug;25(7):501-10
pubmed: 21537945
Ann Surg. 2007 Dec;246(6):932-7; discussion 937-9
pubmed: 18043094
J Clin Pathol. 2008 Dec;61(12):1303-13
pubmed: 18703569
Pancreas. 2016 Aug;45(7):974-9
pubmed: 26692443
Eur J Radiol. 2016 Oct;85(10):1804-1810
pubmed: 27666620
Science. 2009 May 22;324(5930):1029-33
pubmed: 19460998
Clin Gastroenterol Hepatol. 2013 Feb;11(2):181-6
pubmed: 23142206
Cell. 2017 Mar 9;168(6):960-976
pubmed: 28283069
Pancreas. 2008 Nov;37(4):426-31
pubmed: 18953257
Hum Pathol. 2017 Jul;65:71-78
pubmed: 28412205
Gynecol Oncol. 2016 Jul;142(1):62-69
pubmed: 27103175
Ann Surg Oncol. 2017 Jul;24(7):2040-2046
pubmed: 28180987
J Gastroenterol. 2005 Jul;40(7):669-75
pubmed: 16082582
Pancreatology. 2017 Nov - Dec;17(6):911-919
pubmed: 29033011
J Am Coll Surg. 2015 Jul;221(1):48-56
pubmed: 26095551
Leukemia. 2017 Nov;31(11):2326-2335
pubmed: 28280275
Cancer. 1997 Sep 15;80(6):1046-51
pubmed: 9305704
Cancer Sci. 2016 Dec;107(12):1919-1928
pubmed: 27699948