Bad phosphorylation as a target of inhibition in oncology

Ngoc Linh Chi Bui; Vijay Pandey; Tao Zhu; Lan Ma; Basappa; Peter E. Lobie

doi:10.1016/j.canlet.2017.11.017

Bad phosphorylation as a target of inhibition in oncology

Ngoc Linh Chi Bui, Vijay Pandey, Tao Zhu, Lan Ma, Basappa, Peter E. Lobie

Research output: Contribution to journal › Review article › peer-review

55 Scopus citations

Abstract

Bcl-2 agonist of cell death (BAD) is a BH3-only member of the Bcl-2 family which possesses important regulatory function in apoptosis. BAD has also been shown to possess many non-apoptotic functions closely linked to cancer including regulation of glycolysis, autophagy, cell cycle progression and immune system development. Interestingly, BAD can be either pro-apoptotic or pro-survival depending on the phosphorylation state of three specific serine residues (human S75, S99 and S118). Expression of BAD and BAD phosphorylation patterns have been shown to influence tumor initiation and progression and play a predictive role in disease prognosis, drug response and chemosensitivity in various cancers. This review aims to summarize the current evidence on the functional role of BAD phosphorylation in human cancer and evaluate the potential utility of modulating BAD phosphorylation in cancer.

Original language	English (US)
Pages (from-to)	177-186
Number of pages	10
Journal	Cancer Letters
Volume	415
DOIs	https://doi.org/10.1016/j.canlet.2017.11.017
State	Published - Feb 28 2018

Keywords

Apoptosis
BAD phosphorylation
Bcl-2 family
kinase inhibitor

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1016/j.canlet.2017.11.017

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title = "Bad phosphorylation as a target of inhibition in oncology",

abstract = "Bcl-2 agonist of cell death (BAD) is a BH3-only member of the Bcl-2 family which possesses important regulatory function in apoptosis. BAD has also been shown to possess many non-apoptotic functions closely linked to cancer including regulation of glycolysis, autophagy, cell cycle progression and immune system development. Interestingly, BAD can be either pro-apoptotic or pro-survival depending on the phosphorylation state of three specific serine residues (human S75, S99 and S118). Expression of BAD and BAD phosphorylation patterns have been shown to influence tumor initiation and progression and play a predictive role in disease prognosis, drug response and chemosensitivity in various cancers. This review aims to summarize the current evidence on the functional role of BAD phosphorylation in human cancer and evaluate the potential utility of modulating BAD phosphorylation in cancer.",

keywords = "Apoptosis, BAD phosphorylation, Bcl-2 family, kinase inhibitor",

author = "Bui, {Ngoc Linh Chi} and Vijay Pandey and Tao Zhu and Lan Ma and Basappa and Lobie, {Peter E.}",

note = "Funding Information: This work was funded by The Cancer Science Institute of Singapore through grants from the National Research Foundation and Ministry of Education, Singapore and National Research Foundation, Singapore (Grant No. R-713-000-163-511 ) and by a grant from the National Medical Research Council of Singapore (Grants R-713-000-206-511 ). PEL was also supported by The Chinese Academy of Sciences President's International Fellowship Initiative (PIFI) Grant No. 2015VBA031 . Publisher Copyright: {\textcopyright} 2017 Elsevier B.V.",

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doi = "10.1016/j.canlet.2017.11.017",

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AU - Bui, Ngoc Linh Chi

AU - Pandey, Vijay

AU - Zhu, Tao

AU - Ma, Lan

AU - Basappa,

AU - Lobie, Peter E.

N1 - Funding Information: This work was funded by The Cancer Science Institute of Singapore through grants from the National Research Foundation and Ministry of Education, Singapore and National Research Foundation, Singapore (Grant No. R-713-000-163-511 ) and by a grant from the National Medical Research Council of Singapore (Grants R-713-000-206-511 ). PEL was also supported by The Chinese Academy of Sciences President's International Fellowship Initiative (PIFI) Grant No. 2015VBA031 . Publisher Copyright: © 2017 Elsevier B.V.

PY - 2018/2/28

Y1 - 2018/2/28

N2 - Bcl-2 agonist of cell death (BAD) is a BH3-only member of the Bcl-2 family which possesses important regulatory function in apoptosis. BAD has also been shown to possess many non-apoptotic functions closely linked to cancer including regulation of glycolysis, autophagy, cell cycle progression and immune system development. Interestingly, BAD can be either pro-apoptotic or pro-survival depending on the phosphorylation state of three specific serine residues (human S75, S99 and S118). Expression of BAD and BAD phosphorylation patterns have been shown to influence tumor initiation and progression and play a predictive role in disease prognosis, drug response and chemosensitivity in various cancers. This review aims to summarize the current evidence on the functional role of BAD phosphorylation in human cancer and evaluate the potential utility of modulating BAD phosphorylation in cancer.

AB - Bcl-2 agonist of cell death (BAD) is a BH3-only member of the Bcl-2 family which possesses important regulatory function in apoptosis. BAD has also been shown to possess many non-apoptotic functions closely linked to cancer including regulation of glycolysis, autophagy, cell cycle progression and immune system development. Interestingly, BAD can be either pro-apoptotic or pro-survival depending on the phosphorylation state of three specific serine residues (human S75, S99 and S118). Expression of BAD and BAD phosphorylation patterns have been shown to influence tumor initiation and progression and play a predictive role in disease prognosis, drug response and chemosensitivity in various cancers. This review aims to summarize the current evidence on the functional role of BAD phosphorylation in human cancer and evaluate the potential utility of modulating BAD phosphorylation in cancer.

KW - Apoptosis

KW - BAD phosphorylation

KW - Bcl-2 family

KW - kinase inhibitor

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DO - 10.1016/j.canlet.2017.11.017

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VL - 415

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JO - Cancer Letters

JF - Cancer Letters

ER -

Bad phosphorylation as a target of inhibition in oncology

Abstract

Keywords

ASJC Scopus subject areas

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