Upregulated CD58 is associated with clinicopathological characteristics and poor prognosis of patients with pancreatic ductal adenocarcinoma.
CD58
Immune infiltration
Pancreatic ductal adenocarcinoma
Prognosis
Survival
Journal
Cancer cell international
ISSN: 1475-2867
Titre abrégé: Cancer Cell Int
Pays: England
ID NLM: 101139795
Informations de publication
Date de publication:
30 Jun 2021
30 Jun 2021
Historique:
received:
29
03
2021
accepted:
21
06
2021
entrez:
1
7
2021
pubmed:
2
7
2021
medline:
2
7
2021
Statut:
epublish
Résumé
CD58 has been demonstrated to be abnormally expressed in multiple hematopoietic malignancies and solid tumors and plays an essential role in tumorigenesis and progression; however, its clinical significance and prognostic value in pancreatic ductal adenocarcinoma (PDAC) remain unknown. Based on diverse online public databases and 81 PDAC samples of tissue microarray-based immunohistochemistry (IHC), we evaluated CD58 expression in PDAC patients and analyzed its association with clinicopathological characteristics, clinical outcomes, and infiltration of immune cells in PDAC. Furthermore, the correlation between CD58 and the cancer stem cell (CSC)-related, epithelial-mesenchymal transition (EMT)-related, and immune-related markers were detected. Besides, the functional enrichment analysis and related pathways were analyzed and visualized. CD58 expression was elevated in pancreatitis and PDAC tissues than normal pancreas or adjacent nontumor tissues. The positive cases of CD58 (e.g. more than 50% positive cells) in PDAC account for 95.06% (77/81). Upregulated CD58 in cancer tissues was associated with worse histological grade, larger tumor size, and poorer overall survival and disease-free survival in PDAC patients. Furthermore, Cox multivariate regression analysis revealed that CD58 was an independent prognostic factor in PDAC. CD58 expression was correlated with infiltrations of neutrophils, CD8 CD58 expression is upregulated in PDAC tissues and its high expression is notably related to poor survival of PDAC. Therefore, CD58 may serve as a novel and effective marker for predicting the prognosis of PDAC patients.
Sections du résumé
BACKGROUND
BACKGROUND
CD58 has been demonstrated to be abnormally expressed in multiple hematopoietic malignancies and solid tumors and plays an essential role in tumorigenesis and progression; however, its clinical significance and prognostic value in pancreatic ductal adenocarcinoma (PDAC) remain unknown.
METHODS
METHODS
Based on diverse online public databases and 81 PDAC samples of tissue microarray-based immunohistochemistry (IHC), we evaluated CD58 expression in PDAC patients and analyzed its association with clinicopathological characteristics, clinical outcomes, and infiltration of immune cells in PDAC. Furthermore, the correlation between CD58 and the cancer stem cell (CSC)-related, epithelial-mesenchymal transition (EMT)-related, and immune-related markers were detected. Besides, the functional enrichment analysis and related pathways were analyzed and visualized.
RESULTS
RESULTS
CD58 expression was elevated in pancreatitis and PDAC tissues than normal pancreas or adjacent nontumor tissues. The positive cases of CD58 (e.g. more than 50% positive cells) in PDAC account for 95.06% (77/81). Upregulated CD58 in cancer tissues was associated with worse histological grade, larger tumor size, and poorer overall survival and disease-free survival in PDAC patients. Furthermore, Cox multivariate regression analysis revealed that CD58 was an independent prognostic factor in PDAC. CD58 expression was correlated with infiltrations of neutrophils, CD8
CONCLUSIONS
CONCLUSIONS
CD58 expression is upregulated in PDAC tissues and its high expression is notably related to poor survival of PDAC. Therefore, CD58 may serve as a novel and effective marker for predicting the prognosis of PDAC patients.
Identifiants
pubmed: 34193136
doi: 10.1186/s12935-021-02037-0
pii: 10.1186/s12935-021-02037-0
pmc: PMC8243423
doi:
Types de publication
Journal Article
Langues
eng
Pagination
327Subventions
Organisme : National Natural Science Foundation of China
ID : 81872501
Organisme : National Natural Science Foundation of China
ID : 81673023
Organisme : National Natural Science Foundation of China
ID : 81272573
Organisme : National Natural Science Foundation of China
ID : 81502068
Organisme : Natural Science Foundation of Beijing Municipality
ID : 7172177
Références
Am J Transl Res. 2018 Nov 15;10(11):3514-3528
pubmed: 30662604
Med Oncol. 2015 Jun;32(6):616
pubmed: 25920608
Sci Rep. 2018 Jun 15;8(1):9227
pubmed: 29907753
Nature. 1986 Sep 18-24;323(6085):262-4
pubmed: 3093887
Nucleic Acids Res. 2010 Jul;38(Web Server issue):W214-20
pubmed: 20576703
Trends Biochem Sci. 2018 Dec;43(12):1014-1032
pubmed: 30287140
Br J Cancer. 1990 Oct;62(4):603-6
pubmed: 1699592
Leuk Res. 2016 Apr;43:33-8
pubmed: 26930456
J Immunol. 1983 Aug;131(2):611-6
pubmed: 6345670
Oncotarget. 2016 Dec 13;7(50):83294-83307
pubmed: 27825110
Nature. 1987 Oct 29-Nov 4;329(6142):846-8
pubmed: 3313053
J Clin Invest. 1991 Dec;88(6):2131-6
pubmed: 1721627
Int J Cancer Suppl. 1991;6:155-62
pubmed: 1712347
Nucleic Acids Res. 2017 Jul 3;45(W1):W98-W102
pubmed: 28407145
Cancer Cell Int. 2018 Jun 18;18:85
pubmed: 29946224
Mol Immunol. 2020 Mar;119:35-45
pubmed: 31962268
Mol Cell Proteomics. 2014 Feb;13(2):397-406
pubmed: 24309898
Lancet. 2016 Jul 2;388(10039):73-85
pubmed: 26830752
Cancer Res. 2017 Nov 1;77(21):e108-e110
pubmed: 29092952
Int J Cancer. 1995 Dec 20;64(6):415-23
pubmed: 8550244
Cancer Res. 1993 Jul 15;53(14):3343-8
pubmed: 7686816
Lancet Oncol. 2020 Mar;21(3):e135-e145
pubmed: 32135117
Cancer Cell. 2011 Dec 13;20(6):728-40
pubmed: 22137796
J Immunol. 1992 Apr 1;148(7):2023-9
pubmed: 1372020
Cell. 1999 Jun 11;97(6):791-803
pubmed: 10380930
J Cancer. 2018 Oct 20;9(22):4215-4222
pubmed: 30519322
Cancer Res. 2017 Aug 1;77(15):4158-4170
pubmed: 28611041
Cell Death Dis. 2019 Nov 4;10(11):836
pubmed: 31685825
Oncogene. 2004 Sep 16;23(42):7095-103
pubmed: 15258566
J Neuroimmunol. 1990 Sep-Oct;29(1-3):229-38
pubmed: 1698816
Nature. 2015 Feb 26;518(7540):495-501
pubmed: 25719666
J Cancer. 2020 Feb 3;11(8):2213-2221
pubmed: 32127948
Nat Genet. 2000 May;25(1):25-9
pubmed: 10802651
Cancer Res. 2014 Jun 1;74(11):2913-21
pubmed: 24840647
J Exp Clin Cancer Res. 2020 Nov 4;39(1):231
pubmed: 33148302
Bioinformatics. 2012 Jul 1;28(13):1805-6
pubmed: 22543366
Proc Natl Acad Sci U S A. 1982 Dec;79(23):7489-93
pubmed: 6984191
PLoS One. 2013 Sep 16;8(9):e74250
pubmed: 24066126
Nat Rev Immunol. 2018 Nov;18(11):671-688
pubmed: 30209347
Nat Genet. 2021 Mar;53(3):332-341
pubmed: 33649592
J Cancer. 2018 Jun 23;9(15):2713-2722
pubmed: 30087712
Oncogene. 2015 Mar 19;34(12):1520-31
pubmed: 24727892
Blood. 1992 Jan 1;79(1):138-43
pubmed: 1370201
Proc Natl Acad Sci U S A. 1989 Jul;86(14):5557-61
pubmed: 2473473
Clin Cancer Res. 2005 May 1;11(9):3587-96
pubmed: 15867264
Br J Cancer. 2013 Mar 5;108(4):914-23
pubmed: 23385730
J Exp Clin Cancer Res. 2018 Jul 28;37(1):175
pubmed: 30055645
Nucleic Acids Res. 2000 Jan 1;28(1):27-30
pubmed: 10592173
CA Cancer J Clin. 2018 Nov;68(6):394-424
pubmed: 30207593
Blood. 1990 May 1;75(9):1827-33
pubmed: 1691936
Neoplasia. 2004 Jan-Feb;6(1):1-6
pubmed: 15068665
Nature. 1987 Oct 29-Nov 4;329(6142):840-2
pubmed: 3313052
Nucleic Acids Res. 2018 Jan 4;46(D1):D956-D963
pubmed: 29136207
J Transl Med. 2017 Jul 3;15(1):152
pubmed: 28673320
Sci Rep. 2015 Nov 04;5:16067
pubmed: 26530532