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Article ; Online: Discovery, development and application of drugs targeting BCL-2 pro-survival proteins in cancer.

Lee, Erinna F / Fairlie, W Douglas

2021 Volume 49, Issue 5, Page(s) 2381–2395

Abstract: The discovery of a new class of small molecule compounds that target the BCL-2 family of anti-apoptotic proteins is one of the great success stories of basic science leading to translational outcomes in the last 30 years. The eponymous BCL-2 protein was ... ...

Abstract	The discovery of a new class of small molecule compounds that target the BCL-2 family of anti-apoptotic proteins is one of the great success stories of basic science leading to translational outcomes in the last 30 years. The eponymous BCL-2 protein was identified over 30 years ago due to its association with cancer. However, it was the unveiling of the biochemistry and structural biology behind it and its close relatives' mechanism(s)-of-action that provided the inspiration for what are now known as 'BH3-mimetics', the first clinically approved drugs designed to specifically inhibit protein-protein interactions. Herein, we chart the history of how these drugs were discovered, their evolution and application in cancer treatment.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Drug Delivery Systems ; Drug Discovery ; Humans ; Ligands ; Molecular Mimicry ; Proto-Oncogene Proteins c-bcl-2/drug effects
Chemical Substances	Antineoplastic Agents ; BCL2 protein, human ; Ligands ; Proto-Oncogene Proteins c-bcl-2
Language	English
Publishing date	2021-09-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20210749
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Targeting the BCL-2-regulated apoptotic pathway for the treatment of solid cancers.

Fairlie, W Douglas / Lee, Erinna F

Biochemical Society transactions

2021 Volume 49, Issue 5, Page(s) 2397–2410

Abstract: The deregulation of apoptosis is a key contributor to tumourigenesis as it can lead to the unwanted survival of rogue cells. Drugs known as the BH3-mimetics targeting the pro-survival members of the BCL-2 protein family to induce apoptosis in cancer ... ...

Abstract	The deregulation of apoptosis is a key contributor to tumourigenesis as it can lead to the unwanted survival of rogue cells. Drugs known as the BH3-mimetics targeting the pro-survival members of the BCL-2 protein family to induce apoptosis in cancer cells have achieved clinical success for the treatment of haematological malignancies. However, despite our increasing knowledge of the pro-survival factors mediating the unwanted survival of solid tumour cells, and our growing BH3-mimetics armamentarium, the application of BH3-mimetic therapy in solid cancers has not reached its full potential. This is mainly attributed to the need to identify clinically safe, yet effective, combination strategies to target the multiple pro-survival proteins that typically mediate the survival of solid tumours. In this review, we discuss current and exciting new developments in the field that has the potential to unleash the full power of BH3-mimetic therapy to treat currently recalcitrant solid malignancies.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Apoptosis ; Cell Line, Tumor ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism
Chemical Substances	Antineoplastic Agents ; Proto-Oncogene Proteins c-bcl-2
Language	English
Publishing date	2021-10-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20210750
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Co-Operativity between MYC and BCL-2 Pro-Survival Proteins in Cancer.

Fairlie, Walter Douglas / Lee, Erinna F

International journal of molecular sciences

2021 Volume 22, Issue 6

Abstract: B-Cell Lymphoma 2 (BCL-2), c-MYC and related proteins are arguably amongst the most widely studied in all of biology. Every year there are thousands of papers reporting on different aspects of their biochemistry, cellular and physiological mechanisms and ...

Abstract	B-Cell Lymphoma 2 (BCL-2), c-MYC and related proteins are arguably amongst the most widely studied in all of biology. Every year there are thousands of papers reporting on different aspects of their biochemistry, cellular and physiological mechanisms and functions. This plethora of literature can be attributed to both proteins playing essential roles in the normal functioning of a cell, and by extension a whole organism, but also due to their central role in disease, most notably, cancer. Many cancers arise due to genetic lesions resulting in deregulation of both proteins, and indeed the development and survival of tumours is often dependent on co-operativity between these protein families. In this review we will discuss the individual roles of both proteins in cancer, describe cancers where co-operativity between them has been well-characterised and finally, some strategies to target these proteins therapeutically.
MeSH term(s)	Aniline Compounds/therapeutic use ; Antineoplastic Agents/therapeutic use ; Apoptosis/drug effects ; Apoptosis/genetics ; Biphenyl Compounds/therapeutic use ; Bridged Bicyclo Compounds, Heterocyclic/therapeutic use ; Carcinogenesis/drug effects ; Carcinogenesis/genetics ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/genetics ; Clinical Trials as Topic ; Gene Expression Regulation, Neoplastic ; Humans ; Morpholinos/therapeutic use ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Nitrophenols/therapeutic use ; Peptide Fragments/therapeutic use ; Piperazines/therapeutic use ; Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Proto-Oncogene Proteins c-myc/antagonists & inhibitors ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Proto-Oncogene Proteins c-myc/therapeutic use ; Rituximab/therapeutic use ; Signal Transduction ; Sulfonamides/therapeutic use
Chemical Substances	ABT-737 ; AVI-4126 ; Aniline Compounds ; Antineoplastic Agents ; BCL2 protein, human ; Biphenyl Compounds ; Bridged Bicyclo Compounds, Heterocyclic ; MYC protein, human ; Morpholinos ; Nitrophenols ; Peptide Fragments ; Piperazines ; Proto-Oncogene Proteins c-bcl-2 ; Proto-Oncogene Proteins c-myc ; Sulfonamides ; omomyc protein ; Rituximab (4F4X42SYQ6) ; venetoclax (N54AIC43PW) ; navitoclax (XKJ5VVK2WD)
Language	English
Publishing date	2021-03-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22062841
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The emerging roles of autophagy in intestinal epithelial cells and its links to inflammatory bowel disease.

Tran, Sharon / Juliani, Juliani / Fairlie, W Douglas / Lee, Erinna F

Biochemical Society transactions

2023 Volume 51, Issue 2, Page(s) 811–826

Abstract: Landmark genome-wide association studies (GWAS) identified that mutations in autophagy genes correlated with inflammatory bowel disease (IBD), a heterogenous disease characterised by prolonged inflammation of the gastrointestinal tract, that can reduce a ...

Abstract	Landmark genome-wide association studies (GWAS) identified that mutations in autophagy genes correlated with inflammatory bowel disease (IBD), a heterogenous disease characterised by prolonged inflammation of the gastrointestinal tract, that can reduce a person's quality of life. Autophagy, the delivery of intracellular components to the lysosome for degradation, is a critical cellular housekeeping process that removes damaged proteins and turns over organelles, recycling their amino acids and other constituents to supply cells with energy and necessary building blocks. This occurs under both basal and challenging conditions such as nutrient deprivation. An understanding of the relationship between autophagy, intestinal health and IBD aetiology has improved over time, with autophagy having a verified role in the intestinal epithelium and immune cells. Here, we discuss research that has led to an understanding that autophagy genes, including ATG16L, ATG5, ATG7, IRGM, and Class III PI3K complex members, contribute to innate immune defence in intestinal epithelial cells (IECs) via selective autophagy of bacteria (xenophagy), how autophagy contributes to the regulation of the intestinal barrier via cell junctional proteins, and the critical role of autophagy genes in intestinal epithelial secretory subpopulations, namely Paneth and goblet cells. We also discuss how intestinal stem cells can utilise autophagy. Importantly, mouse studies have provided evidence that autophagy deregulation has serious physiological consequences including IEC death and intestinal inflammation. Thus, autophagy is now established as a key regulator of intestinal homeostasis. Further research into how its cytoprotective mechanisms can prevent intestinal inflammation may provide insights into the effective management of IBD.
MeSH term(s)	Animals ; Mice ; Genome-Wide Association Study ; Quality of Life ; Inflammatory Bowel Diseases ; Epithelial Cells/metabolism ; Intestinal Mucosa ; Inflammation/metabolism ; Autophagy/genetics
Language	English
Publishing date	2023-04-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20221300
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: BECLIN1

Sharon Tran / W. Douglas Fairlie / Erinna F. Lee

Cells, Vol 10, Iss 1522, p

Protein Structure, Function and Regulation

2021 Volume 1522

Abstract: BECLIN1 is a well-established regulator of autophagy, a process essential for mammalian survival. It functions in conjunction with other proteins to form Class III Phosphoinositide 3-Kinase (PI3K) complexes to generate phosphorylated phosphatidylinositol ...

Abstract	BECLIN1 is a well-established regulator of autophagy, a process essential for mammalian survival. It functions in conjunction with other proteins to form Class III Phosphoinositide 3-Kinase (PI3K) complexes to generate phosphorylated phosphatidylinositol (PtdIns), lipids essential for not only autophagy but other membrane trafficking processes. Over the years, studies have elucidated the structural, biophysical, and biochemical properties of BECLIN1, which have shed light on how this protein functions to allosterically regulate these critical processes of autophagy and membrane trafficking. Here, we review these findings and how BECLIN1’s diverse protein interactome regulates it, as well as its impact on organismal physiology.
Keywords	BECLIN1 ; PI3K Class III complexes ; autophagy ; BCL-2 ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: BECLIN1: Protein Structure, Function and Regulation.

Tran, Sharon / Fairlie, W Douglas / Lee, Erinna F

Cells

2021 Volume 10, Issue 6

Abstract	BECLIN1 is a well-established regulator of autophagy, a process essential for mammalian survival. It functions in conjunction with other proteins to form Class III Phosphoinositide 3-Kinase (PI3K) complexes to generate phosphorylated phosphatidylinositol (PtdIns), lipids essential for not only autophagy but other membrane trafficking processes. Over the years, studies have elucidated the structural, biophysical, and biochemical properties of BECLIN1, which have shed light on how this protein functions to allosterically regulate these critical processes of autophagy and membrane trafficking. Here, we review these findings and how BECLIN1's diverse protein interactome regulates it, as well as its impact on organismal physiology.
MeSH term(s)	Animals ; Beclin-1 ; Humans
Chemical Substances	Beclin-1
Language	English
Publishing date	2021-06-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10061522
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Co-Operativity between MYC and BCL-2 Pro-Survival Proteins in Cancer

W. Douglas Fairlie / Erinna F. Lee

International Journal of Molecular Sciences, Vol 22, Iss 2841, p

2021 Volume 2841

Abstract	B-Cell Lymphoma 2 (BCL-2), c-MYC and related proteins are arguably amongst the most widely studied in all of biology. Every year there are thousands of papers reporting on different aspects of their biochemistry, cellular and physiological mechanisms and functions. This plethora of literature can be attributed to both proteins playing essential roles in the normal functioning of a cell, and by extension a whole organism, but also due to their central role in disease, most notably, cancer. Many cancers arise due to genetic lesions resulting in deregulation of both proteins, and indeed the development and survival of tumours is often dependent on co-operativity between these protein families. In this review we will discuss the individual roles of both proteins in cancer, describe cancers where co-operativity between them has been well-characterised and finally, some strategies to target these proteins therapeutically.
Keywords	apoptosis ; MYC ; BCL-2 ; BH3-only ; BH3-mimetic ; pro-survival ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The Structural Biology of Bcl-x

Lee, Erinna F / Fairlie, W Douglas

International journal of molecular sciences

2019 Volume 20, Issue 9

Abstract: Interactions between the pro-survival and pro-apoptotic members of the Bcl-2 family of proteins dictate whether a cell lives or dies. Much of our knowledge of the molecular details of these interactions has come from biochemical and structural studies on ...

Abstract	Interactions between the pro-survival and pro-apoptotic members of the Bcl-2 family of proteins dictate whether a cell lives or dies. Much of our knowledge of the molecular details of these interactions has come from biochemical and structural studies on the pro-survival protein Bcl-x
MeSH term(s)	Animals ; Binding Sites ; Humans ; Protein Binding ; Protein Multimerization ; Tumor Suppressor Protein p53/chemistry ; Tumor Suppressor Protein p53/metabolism ; bcl-X Protein/chemistry ; bcl-X Protein/metabolism
Chemical Substances	Tumor Suppressor Protein p53 ; bcl-X Protein
Language	English
Publishing date	2019-05-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20092234
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Article: Crosstalk between apoptosis and autophagy signaling pathways.

Fairlie, W Douglas / Tran, Sharon / Lee, Erinna F

International review of cell and molecular biology

2020 Volume 352, Page(s) 115–158

Abstract: The fate of a cell is determined by multiple signaling pathways in response to a range of stimuli. Probably the most prominent cell death mechanism is apoptosis which can be triggered by both internal stresses, as well as extracellular stimuli, and is ... ...

Abstract	The fate of a cell is determined by multiple signaling pathways in response to a range of stimuli. Probably the most prominent cell death mechanism is apoptosis which can be triggered by both internal stresses, as well as extracellular stimuli, and is executed by two well-characterized pathways, the intrinsic and the extrinsic apoptosis pathways. Although autophagy can also lead to cell death under certain circumstances, its major function is as a cell survival process. Given that the life of a cell is at stake, it is not surprising that there is significant molecular crosstalk between these pathways. The nature of these interconnections is diverse and ranges from protein-protein interactions and post-translational modifications through to the degradation of molecular components by different proteins and organelles. In this chapter we review these mechanisms in detail.
MeSH term(s)	Animals ; Apoptosis ; Apoptosis Regulatory Proteins/metabolism ; Autophagy ; Caspase 8/metabolism ; Humans ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Signal Transduction
Chemical Substances	Apoptosis Regulatory Proteins ; Proto-Oncogene Proteins c-bcl-2 ; Caspase 8 (EC 3.4.22.-)
Language	English
Publishing date	2020-02-05
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2427220-6
ISSN	1937-6448 ; 0074-7696
ISSN	1937-6448 ; 0074-7696
DOI	10.1016/bs.ircmb.2020.01.003
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Article ; Online: The role of BCL-2 family proteins and therapeutic potential of BH3-mimetics in malignant pleural mesothelioma.

Arulananda, Surein / Lee, Erinna F / Fairlie, W Douglas / John, Thomas

Expert review of anticancer therapy

2020 Volume 21, Issue 4, Page(s) 413–424

Abstract: Introduction: ...

Abstract	Introduction:
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Biomimetic Materials/pharmacology ; Cell Survival ; Humans ; Mesothelioma/drug therapy ; Mesothelioma/pathology ; Molecular Targeted Therapy ; Pleural Neoplasms/drug therapy ; Pleural Neoplasms/pathology ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Survival Rate
Chemical Substances	Antineoplastic Agents ; Proto-Oncogene Proteins c-bcl-2
Language	English
Publishing date	2020-12-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2112544-2
ISSN	1744-8328 ; 1473-7140
ISSN (online)	1744-8328
ISSN	1473-7140
DOI	10.1080/14737140.2021.1856660
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