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B7H3 As a Promoter of Metastasis and Promising Therapeutic Target

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/71062

Title: B7H3 As a Promoter of Metastasis and Promising Therapeutic Target
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: B7H3
CD276
metastasis
epithelial-to-mesenchymal transition
cancer stem cells
microRNA
Issue Date: 6-Jul-2018
Publisher: Frontiers Media
Journal Title: Frontiers in Oncology
Volume: 8
Start Page: 264
Publisher DOI: 10.3389/fonc.2018.00264
Abstract: B7H3 (also known as CD276, an immune checkpoint molecule) is aberrantly overexpressed in many types of cancer, and such upregulation is generally associated with a poor clinical prognosis. Recent discoveries indicate a crucial role for B7H3 in promoting carcinogenesis and metastasis. This review will focus on the latest developments relating specifically to the oncogenic activity of B7H3 and will describe the upstream regulators and downstream effectors of B7H3 in cancer. Finally, we discuss the emerging roles of microRNAs (miRNAs) in inhibiting B7H3-mediated tumor promotion. Excellent recent studies have shed new light on the functions of B7H3 in cancer and identified B7H3 as a critical promoter of tumor cell proliferation, migration, invasion, epithelial-to-mesenchymal transition, cancer stemness, drug resistance, and the Warburg effect. Numerous miRNAs are reported to regulate the expression of B7H3. Our meta-analysis of miRNA database revealed that 17 common miRNAs potentially interact with B7H3 mRNA. The analysis of the TCGA ovarian cancer dataset indicated that low miR-187 and miR-489 expression was associated with poor prognosis. Future studies aimed at delineating the precise cellular and molecular mechanisms underpinning B7H3-mediated tumor promotion will provide further insights into the cell biology of tumor development. In addition, inhibition of B7H3 signaling, to be used alone or in combination with other treatments, will contribute to improvements in clinical practice and benefit cancer patients.
Rights: https://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/71062
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

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