Mitochondrial expression of the DNA repair enzyme OGG1 improves the prognosis of pancreatic ductal adenocarcinoma.


Journal

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
ISSN: 1424-3911
Titre abrégé: Pancreatology
Pays: Switzerland
ID NLM: 100966936

Informations de publication

Date de publication:
Sep 2020
Historique:
received: 29 02 2020
revised: 05 07 2020
accepted: 17 07 2020
pubmed: 4 8 2020
medline: 27 8 2021
entrez: 4 8 2020
Statut: ppublish

Résumé

8-Hydroxydeoxyguanosine (8-OHdG) is an indicator of oxidative stress and causes transversion mutations and carcinogenesis. 8-OHdG is excision repaired by 8-OHdG DNA glycosylase 1 (OGG1), which is classified as nuclear and mitochondrial subtypes. We aimed to clarify the role of OGG1 in pancreatic ductal adenocarcinoma (PDAC). Ninety-two patients with PDAC who had undergone surgical resection at multiple institutions were immunohistochemically analyzed. The OGG1 and 8-OHdG expression levels were scored using the Germann Immunoreactive Score. The cutoff values of OGG1, as well as that of 8-OHdG, were determined. The low nuclear OGG1 expression group (n = 41) showed significantly higher carbohydrate antigen (CA)19-9 (p = 0.026), and higher s-pancreas antigen (SPAN)-1 (p = 0.017) than the high expression group (n = 51). Nuclear OGG1 expression has no effect on the prognosis. The low mitochondrial OGG1 expression group (n = 40) showed higher CA19-9 (p = 0.041), higher SPAN-1 (p = 0.032), and more histological perineural invasion (p = 0.037) than the high expression group (n = 52). The low mitochondrial OGG1 expression group had a significantly shorter recurrence-free survival (p = 0.0080) and overall survival (p = 0.0073) rates. The Cox proportional hazards model revealed that low mitochondrial OGG1 expression is an independent risk factor of the PDAC prognosis. OGG1 expression was negatively correlated with 8-OHdG expression (p = 0.0004), and high 8-OHdG expression shortened the recurrence-free survival of patients with PDAC. Low mitochondrial OGG1 expression might aggravate the PDAC prognosis.

Sections du résumé

BACKGROUND/OBJECTIVES OBJECTIVE
8-Hydroxydeoxyguanosine (8-OHdG) is an indicator of oxidative stress and causes transversion mutations and carcinogenesis. 8-OHdG is excision repaired by 8-OHdG DNA glycosylase 1 (OGG1), which is classified as nuclear and mitochondrial subtypes. We aimed to clarify the role of OGG1 in pancreatic ductal adenocarcinoma (PDAC).
METHODS METHODS
Ninety-two patients with PDAC who had undergone surgical resection at multiple institutions were immunohistochemically analyzed. The OGG1 and 8-OHdG expression levels were scored using the Germann Immunoreactive Score. The cutoff values of OGG1, as well as that of 8-OHdG, were determined.
RESULTS RESULTS
The low nuclear OGG1 expression group (n = 41) showed significantly higher carbohydrate antigen (CA)19-9 (p = 0.026), and higher s-pancreas antigen (SPAN)-1 (p = 0.017) than the high expression group (n = 51). Nuclear OGG1 expression has no effect on the prognosis. The low mitochondrial OGG1 expression group (n = 40) showed higher CA19-9 (p = 0.041), higher SPAN-1 (p = 0.032), and more histological perineural invasion (p = 0.037) than the high expression group (n = 52). The low mitochondrial OGG1 expression group had a significantly shorter recurrence-free survival (p = 0.0080) and overall survival (p = 0.0073) rates. The Cox proportional hazards model revealed that low mitochondrial OGG1 expression is an independent risk factor of the PDAC prognosis. OGG1 expression was negatively correlated with 8-OHdG expression (p = 0.0004), and high 8-OHdG expression shortened the recurrence-free survival of patients with PDAC.
CONCLUSIONS CONCLUSIONS
Low mitochondrial OGG1 expression might aggravate the PDAC prognosis.

Identifiants

pubmed: 32741713
pii: S1424-3903(20)30226-X
doi: 10.1016/j.pan.2020.07.011
pii:
doi:

Substances chimiques

CA-19-9 Antigen 0
8-Hydroxy-2'-Deoxyguanosine 88847-89-6
DNA Glycosylases EC 3.2.2.-
oxoguanine glycosylase 1, human EC 3.2.2.-

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1175-1182

Informations de copyright

Copyright © 2020 IAP and EPC. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare no conflicts of interest.

Auteurs

Shoichi Inokuchi (S)

Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, 812-8582, Fukuoka, Japan.

Shinji Itoh (S)

Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, 812-8582, Fukuoka, Japan. Electronic address: itoshin@surg2.med.kyushu-u.ac.jp.

Tomoharu Yoshizumi (T)

Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, 812-8582, Fukuoka, Japan.

Kyohei Yugawa (K)

Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, 812-8582, Fukuoka, Japan; Department of Anatomic Pathology, Pathological Sciences, Graduate School of Medical Sciences, Kyushu University, 812-8582, Japan.

Shohei Yoshiya (S)

Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, 812-8582, Fukuoka, Japan.

Takeo Toshima (T)

Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, 812-8582, Fukuoka, Japan.

Kazuki Takeishi (K)

Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, 812-8582, Fukuoka, Japan.

Tomohiro Iguchi (T)

Department of Hepatobiliary-Pancreatic Surgery, National Hospital Organization Kyushu Cancer Center, Fukuoka, 811-1395, Japan.

Kensaku Sanefuji (K)

Department of Surgery, Oita Red Cross Hospital, 870-0033, Oita, Japan.

Noboru Harada (N)

Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, 812-8582, Fukuoka, Japan.

Keishi Sugimachi (K)

Department of Hepatobiliary-Pancreatic Surgery, National Hospital Organization Kyushu Cancer Center, Fukuoka, 811-1395, Japan.

Toru Ikegami (T)

Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, 812-8582, Fukuoka, Japan.

Kenichi Kohashi (K)

Department of Anatomic Pathology, Pathological Sciences, Graduate School of Medical Sciences, Kyushu University, 812-8582, Japan.

Kenichi Taguchi (K)

Department of Pathology, National Hospital Organization Kyushu Cancer Center, Fukuoka, 811-1395, Japan.

Hirotoshi Yonemasu (H)

Department of Anatomic Pathology, Oita Red Cross Hospital, 870-0033, Oita, Japan.

Kengo Fukuzawa (K)

Department of Surgery, Oita Red Cross Hospital, 870-0033, Oita, Japan.

Yoshinao Oda (Y)

Department of Anatomic Pathology, Pathological Sciences, Graduate School of Medical Sciences, Kyushu University, 812-8582, Japan.

Masaki Mori (M)

Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, 812-8582, Fukuoka, Japan.

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Classifications MeSH