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Far upstream element-binding protein 1 is up-regulated in pancreatic cancer and modulates immune response by increasing programmed death ligand 1.

Abstract：

:Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer-related death worldwide. So far, almost all treatments are almost ineffective for pancreatic cancer. Thus, there is an urgent need to develop novel therapeutics for pancreatic cancer treatment. Immune checkpoints blockade therapies, including anti-PD-L1 and anti-PD-1, show promising anti-tumor efficacy for a various type of solid tumors. However, pancreatic cancer is disappointed for anti-PD-L1 therapy alone. The expression level of PD-L1 is considered as one of determinant of checkpoint immunotherapy efficacy. The far upstream element-binding protein 1 (FUBP1) is an important transactivator of c-Myc proto-oncogene. Here, we demonstrate that FUBP1 is overexpressed in pancreatic cancer and associated with poor prognosis. Moreover, we show that FUBP1 promotes tumor cell proliferation and migration and regulates the cancer cell immunity by increasing the PD-L1 expression mediated by Myc in pancreatic cancer cells. Taken together, these findings uncover important aspects of the function of FUBP1 in cancer immunity and elucidated the specific mechanism regulating PD-L1 expression. Targeting FUBP1 may be a novel therapeutic strategy to overcome the immunotherapy resistance in pancreatic cancer.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Fan P,Ma J,Jin X

doi

10.1016/j.bbrc.2018.10.009

subject

Has Abstract

pub_date

2018-11-02 00:00:00

pages

830-836

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(18)32145-4

journal_volume

505

pub_type

杂志文章

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