Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2008 Sep;134(9):1021-7.
doi: 10.1007/s00432-008-0364-8. Epub 2008 Mar 18.

B7-H1 up-regulated expression in human pancreatic carcinoma tissue associates with tumor progression

Lei Geng  1 , Dongsheng Huang, Junwei Liu, Yigang Qian, Junfang Deng, Donglin Li, Zhenhua Hu, Jian Zhang, Guoping Jiang, Shusen Zheng
Affiliations

B7-H1 up-regulated expression in human pancreatic carcinoma tissue associates with tumor progression

Lei Geng et al. J Cancer Res Clin Oncol. 2008 Sep.

Abstract

Purpose: Aberrant tumor cell B7-H1 expression, a member of B7 family that can predominantly stimulate interleukin 10 (IL-10) products, contributed to the tumor immune evasion and tumor progression. This study was designed to investigate the expression of B7-H1 and IL-10 in normal pancreas tissues and pancreatic carcinoma samples, and to evaluate clinical significance of B7-H1 expression in pancreatic carcinoma.

Methods: First, the B7-H1 and IL-10 expression in 40 pancreatic carcinoma samples and 8 healthy pancreas specimens using reverse transcription-PCR (RT-PCR) and western-blotting was detected. Localization of B7-H1 and IL-10 was confirmed by immunohistochemical (IHC) staining. Next, the association between B7-H1 expression and tumor differentiation and tumor stage was analyzed. Finally, the correlation between tumor-associated B7-H1 and IL-10 was evaluated.

Results: Pancreatic carcinoma samples demonstrated the up-regulated expression of B7-H1 and IL-10 at mRNA and protein level compared with normal pancreas tissues. IHC staining revealed that B7-H1 and IL-10 was almost localized in tumor cells. Analysis of relationship between B7-H1 and tumor clinicopathological characteristics showed that B7-H1 expression was significantly associated with poor tumor differentiation (P < 0.01) and advanced tumor stage (P < 0.01). Meanwhile, tumor-associated B7-H1 expression was also correlated with IL-10 products (P < 0.01, R (2) = 0.6985, mRNA level; P < 0.01, R (2) = 0.7236, protein level) in tumor cells.

Conclusions: Our findings for the first time demonstrated up-regulated B7-H1 expression in human pancreatic carcinoma tissues, which might play a role in tumor progression and invasiveness. This expression seemed to be related to the ability of B7-H1 to promoting IL-10 secretion.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Identification of B7-H1 and IL-10mRNA transcripts in pancreatic carcinoma and normal pancreas by RT-PCR. Top B7-H1 mRNA was detected at higher level in pancreatic carcinoma tissue (lane 1, 2, 3) compared with normal pancreas tissue (lane 4, 5, 6), P < 0.05. Bottom IL-10mRNA was detected at higher level in pancreatic carcinoma tissue (lane 1, 2, 3) compared with normal pancreas tissue (lane 4, 5, 6), P < 0.01
Fig. 2
Fig. 2
Detection of B7-H1 and IL-10 protein expression in pancreatic carcinoma specimens and normal pancreas specimens by western-blotting. Increased expression of B7-H1 in pancreatic carcinoma tissues (top lane 1, 2, 3) was observed compared with normal pancreas tissues (top lane 4, 5, 6). IL-10 expression was also significantly increasing in pancreatic carcinoma tissue (middle lane 1, 2, 3) compared with normal pancreatic tissue (middle lane 4, 5, 6)
Fig. 3
Fig. 3
IHC analysis of B7-H1 and IL-10 expression in paraflin-embedded sections of pancreatic carcinoma and normal pancreas. Magnification of a–f ×400. Pancreatic carcinoma tissue showed high intense staining for B7-H1 (b arrow) and IL-10 (e arrow). In normal pancreas tissue, only islets cells showed positively staining for B7-H1 (c arrow) and IL-10 (f arrow). B7-H1 and IL-10 immunoreactive cells were localized in the cytoplasm. Negative control, in which the primary B7-H1 (a) and IL-10 (d) detecting Ab was replaced by 3% BSA/PBS serum, showed complete lack of immunoreactivity
Fig. 4
Fig. 4
Correlation of B7-H1 expression with IL-10 level in pancreatic carcinoma. a The B7-H1 expression was significantly correlated with IL-10 level at mRNA level in pancreatic carcinoma samples (P < 0.01, R 2 = 0.6985). b The B7-H1 expression was significantly correlated with IL-10 level at protein level in pancreatic carcinoma samples (P < 0.01, R 2 = 0.7236)
See this image and copyright information in PMC

References

    1. Akdis CA, Blaser K (2001) Mechanisms of interleukin-10-mediated immune suppression. Immunology 103:131–148 - PMC - PubMed
    1. Bellone G., Turletti A, Artusio E, Mareschi K, Carbone A, Tibaudi D, Robecchi A, Emanuelli G., Rodeck U (1999) Tumor-associated transforming growth factor-ß and interleukin-10 contribute to a systemic Th2 immune phenotype in pancreatic carcinoma patients. Am J Pathol 155:537–547 - PMC - PubMed
    1. Carter L, Fouser LA, Jussif J, Fitz L, Deng B, Wood CR, Collins M, Honjo T, Freeman GJ, Carreno BM (2002) PD-1: PD-L inhibitory pathway affects both CD4(+) and CD8(+) T cells and is overcome by IL-2. Eur J Immunol 32:634–643 - PubMed
    1. Curiel TJ, Wei S, Dong H, Alvarez X, Cheng P, Mottram P, Krzysiek R, Knutson KL, Daniel B, Zimmermann MC, David O, Burow M, Gordon A, Dhurandhar N, Myers L, Berggren R, Hemminki A, Alvarez RD, Emilie D, Curiel DT, Chen L, Zou W (2003) Blockade of B7-H1 improves myeloid dendritic cell-mediated antitumor immunity. Nat Med 9:562–567 - PubMed
    1. Dong H, Zhu G., Tamada K, Chen L (1999) B7-H1, a third member of the B7 family, co-stimulates T-cell proliferation and interleukin-10 secretion. Nat Med 5:1365–1369 - PubMed

Publication types

MeSH terms