B7H3 As a Promoter of Metastasis and Promising Therapeutic Target

Peixin Dong; Ying Xiong; Junming Yue; Sharon J. B. Hanley; Hidemichi Watari

doi:10.3389/fonc.2018.00264

B7H3 As a Promoter of Metastasis and Promising Therapeutic Target

Peixin Dong^* (Corresponding Author), Ying Xiong, Junming Yue, Sharon J. B. Hanley, Hidemichi Watari

^*Corresponding author for this work

Applied Health Sciences

Research output: Contribution to journal › Article › peer-review

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.

Original language	English
Article number	264
Number of pages	8
Journal	Frontiers in Oncology
Volume	8
Early online date	6 Jul 2018
DOIs	https://doi.org/10.3389/fonc.2018.00264
Publication status	Published - 6 Jul 2018

Keywords

B7H3
cancer stem cells
CD276
epithelial-to-mesenchymal transition
metastasis
microRNA

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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Copyright © 2018 Dong, Xiong, Yue, Hanley and Watari. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. https://creativecommons.org/licenses/by/4.0/
Final published version, 1.04 MBLicence: CC BY

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title = "B7H3 As a Promoter of Metastasis and Promising Therapeutic Target",

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.",

keywords = "B7H3, cancer stem cells, CD276, epithelial-to-mesenchymal transition, metastasis, microRNA",

author = "Peixin Dong and Ying Xiong and Junming Yue and Hanley, {Sharon J. B.} and Hidemichi Watari",

note = "Funding This work was supported by a grant from JSPS Grant-in-Aid for Scientific Research (C) (16K11123 and 18K09278) and the Science and Technology Planning Project of Guangdong Province, China (2014A020212124).",

year = "2018",

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doi = "10.3389/fonc.2018.00264",

language = "English",

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AU - Dong, Peixin

AU - Xiong, Ying

AU - Yue, Junming

AU - Hanley, Sharon J. B.

AU - Watari, Hidemichi

N1 - Funding This work was supported by a grant from JSPS Grant-in-Aid for Scientific Research (C) (16K11123 and 18K09278) and the Science and Technology Planning Project of Guangdong Province, China (2014A020212124).

PY - 2018/7/6

Y1 - 2018/7/6

N2 - 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.

AB - 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.

KW - B7H3

KW - cancer stem cells

KW - CD276

KW - epithelial-to-mesenchymal transition

KW - metastasis

KW - microRNA

U2 - 10.3389/fonc.2018.00264

DO - 10.3389/fonc.2018.00264

M3 - Article

VL - 8

JO - Frontiers in Oncology

JF - Frontiers in Oncology

SN - 2234-943X

M1 - 264

ER -

B7H3 As a Promoter of Metastasis and Promising Therapeutic Target

Abstract

Keywords

UN SDGs

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