Skip to main content
padlock icon - secure page this page is secure

Overexpression of B7-H1 correlates with malignant cell proliferation in pancreatic cancer

Buy Article:

$42.00 + tax (Refund Policy)

B7-H1, a member of the B7 family of proteins, is hypothesised to play an important role in the immune escape of tumours through its binding to the PD-1 receptor on activated T and B cells. By inducing T lymphocyte apoptosis, tumour cells can suppress an effective antitumour immune response. Although the immunosuppressive effect of B7-H1 has been studied in many tumours, its other biological functions remain unclear. We previously demonstrated a high expression level of this molecule in pancreatic cancer patient samples and its antiapoptotic effect in pancreatic ductal adenocarcinoma (PDA) cells. The aim of the present study was to investigate the possible role of B7-H1 in the proliferation of PDA cells. Functional studies were performed using pancreatic cell lines that were genetically engineered to express high or low levels of B7-H1, and we found that the overexpression of B7-H1 through plasmid transfection in PDA cells promoted cell proliferation. Conversely, the short-hairpin RNA (shRNA) knockdown of B7-H1 inhibited PDA cell proliferation. Further analyses of the cell cycle and cell cycle-related molecules confirmed this result. Taken together, our results indicate that the upregulation of B7-H1 in pancreatic cancer cells promotes proliferation and accelerates carcinogenesis; these data, therefore, provide insights into the effects of B7-H1 overexpression on pancreatic tumour cells.
No Reference information available - sign in for access.
No Citation information available - sign in for access.
No Supplementary Data.
No Article Media
No Metrics

Document Type: Research Article

Affiliations: 1: Department of General Surgery, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310016, P.R. China 2: Biomedical Research Center, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310016, P.R. China

Publication date: March 1, 2014

More about this publication?
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more