HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Medicine / Faculty of Medicine >
Peer-reviewed Journal Articles, etc >

Tumor-Intrinsic PD-L1 Signaling in Cancer Initiation, Development and Treatment : Beyond Immune Evasion

This item is licensed under: Creative Commons Attribution 4.0 International

Files in This Item:
PD-L1_review_final_PDF.pdf7.01 MBPDFView/Open
Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/71646

Title: Tumor-Intrinsic PD-L1 Signaling in Cancer Initiation, Development and Treatment : Beyond Immune Evasion
Authors: Dong, Peixin Browse this author →KAKEN DB
Xiong, Ying Browse this author
Yue, Junming Browse this author
Hanley, Sharon J. B. Browse this author →KAKEN DB
Watari, Hidemichi Browse this author →KAKEN DB
Keywords: PD-L1
CD274
metastasis
EMT
cancer stem cells
microRNA
Issue Date: 19-Sep-2018
Publisher: Frontiers Media
Journal Title: Frontiers in Oncology
Volume: 8
Start Page: 386
Publisher DOI: 10.3389/fonc.2018.00386
Abstract: Although the role of PD-L1 in suppressing the anti-tumor immune response is extensively documented, recent discoveries indicate a distinct tumor-intrinsic role for PD-L1 in modulating epithelial-to-mesenchymal transition (EMT), cancer stem cell (CSC)-like phenotype, metastasis and resistance to therapy. In this review, we will focus on the newly discovered functions of PD-L1 in the regulation of cancer development, describe underlying molecular mechanisms responsible for PD-L1 upregulation and discuss current insights into novel components of PD-L1 signaling. Furthermore, we summarize our current understanding of the link between PD-L1 signaling and the EMT program as well as the CSC state. Tumor cell-intrinsic PD-L1 clearly contributes to cancer stemness, EMT, tumor invasion and chemoresistance in multiple tumor types. Conversely, activation of OCT4 signaling and upregulation of EMT inducer ZEB1 induce PD-L1 expression in cancer cells, thereby suggesting a possible immune evasion mechanism employed by cancer stem cells during metastasis. Our meta-analysis demonstrated that PD-L1 is co-amplified along with MYC, SOX2, N-cadherin and SNAI1 in the TCGA endometrial and ovarian cancer datasets. Further identification of immune-independent PD-L1 functions and characterization of crucial signaling events upstream or downstream of PD-L1 in diverse cancer types and specific cancer subtypes, would provide additional targets and new therapeutic approaches.
Rights: http://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/71646
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 董 培新

Export metadata:

OAI-PMH ( junii2 , jpcoar )

MathJax is now OFF:


 

 - Hokkaido University