Emerging role of BAD and DAD1 as potential targets and biomarkers in cancer

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

As key regulators of apoptosis, BAD and defender against apoptotic cell death 1 (DAD1) are associated with cancer initiation and progression. Multiple studies have demonstrated that BAD and DAD1 serve critical roles in several types of cancer and perform various functions, such as participating in cellular apoptosis, invasion and chemosensitivity, as well as their role in diagnostic/prognostic judgement, etc. Investigating the detailed mechanisms of the cancerous effects of the two proteins will contribute to enriching the options for targeted therapy, and may improve clinical treatment of cancer. The present review summarizes research advances regarding the associations of BAD and DAD1 with cancer, and a hypothesis on the feasible relationship and interaction mechanism between the two proteins is proposed. Furthermore, the present review highlights the potential of the two proteins as therapeutic targets and valuable diagnostic and prognostic biomarkers.

Related collections

Most cited references 107

Record: found
Abstract: found
Article: found

Hallmarks of Cancer: The Next Generation

Douglas Hanahan, Robert A. Weinberg (2011)

The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.

0 comments Cited 11797 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy.

Peter Czabotar, Guillaume Lessene, Andreas Strasser … (2014)

The BCL-2 protein family determines the commitment of cells to apoptosis, an ancient cell suicide programme that is essential for development, tissue homeostasis and immunity. Too little apoptosis can promote cancer and autoimmune diseases; too much apoptosis can augment ischaemic conditions and drive neurodegeneration. We discuss the biochemical, structural and genetic studies that have clarified how the interplay between members of the BCL-2 family on mitochondria sets the apoptotic threshold. These mechanistic insights into the functions of the BCL-2 family are illuminating the physiological control of apoptosis, the pathological consequences of its dysregulation and the promising search for novel cancer therapies that target the BCL-2 family.

0 comments Cited 522 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Life and death partners: apoptosis, autophagy and the cross-talk between them.

A Eisenberg-Lerner, S Bialik, H-U Simon … (2009)

It is not surprising that the demise of a cell is a complex well-controlled process. Apoptosis, the first genetically programmed death process identified, has been extensively studied and its contribution to the pathogenesis of disease well documented. Yet, apoptosis does not function alone to determine a cell's fate. More recently, autophagy, a process in which de novo-formed membrane-enclosed vesicles engulf and consume cellular components, has been shown to engage in a complex interplay with apoptosis. In some cellular settings, it can serve as a cell survival pathway, suppressing apoptosis, and in others, it can lead to death itself, either in collaboration with apoptosis or as a back-up mechanism when the former is defective. The molecular regulators of both pathways are inter-connected; numerous death stimuli are capable of activating either pathway, and both pathways share several genes that are critical for their respective execution. The cross-talk between apoptosis and autophagy is therefore quite complex, and sometimes contradictory, but surely critical to the overall fate of the cell. Furthermore, the cross-talk is a key factor in the outcome of death-related pathologies such as cancer, its development and treatment.

0 comments Cited 385 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): Oncol Lett

Journal ID (iso-abbrev): Oncol Lett

Journal ID (publisher-id): OL

Title: Oncology Letters

Publisher: D.A. Spandidos

ISSN (Print): 1792-1074

ISSN (Electronic): 1792-1082

Publication date (Print): December 2021

Publication date (Electronic): 28 September 2021

Publication date PMC-release: 28 September 2021

Volume: 22

Issue: 6

Electronic Location Identifier: 811

Affiliations

[1 ]First Clinical Medical College, Xinjiang Medical University, Urumqi, Xinjiang Uyghur Autonomous Region 830054, P.R. China

[2 ]Nursing College, Binzhou Medical University, Binzhou, Shandong 264003, P.R. China

[3 ]Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xinjiang Medical University, Urumqi, Xinjiang Uyghur Autonomous Region 830017, P.R. China

Author notes

Correspondence to: Dr Yan Chen, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xinjiang Medical University, 567 Shangde North Road, Urumqi, Xinjiang Uyghur Autonomous Region 830017, P.R. China, E-mail: yanchen@ 123456xjmu.edu.cn

Article

Publisher ID: OL-0-0-13072

DOI: 10.3892/ol.2021.13072

PMC ID: 8503815

PubMed ID: 34671425

SO-VID: b2c612d5-f311-4887-b656-529aa2e9fa8d

License:

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

History

Date received : 09 July 2021

Date accepted : 01 September 2021

Funding

Funded by: Natural Science Foundation of Xinjiang Uygur Autonomous Region

Award ID: 2020D01C171

Funded by: The Key Discipline of the 13th Five-Year Plan (Plateau Discipline) of Xinjiang Uygur Autonomous Region

This review was supported by Natural Science Foundation of Xinjiang Uygur Autonomous Region (grant no. 2020D01C171). The Key Discipline of the 13th Five-Year Plan (Plateau Discipline) of Xinjiang Uygur Autonomous Region also provided support to this study.

Emerging role of BAD and DAD1 as potential targets and biomarkers in cancer

Read this article at

Abstract

Related collections

Karger: Oncology

Most cited references 107

Hallmarks of Cancer: The Next Generation

Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy.

Life and death partners: apoptosis, autophagy and the cross-talk between them.

Author and article information

Journal

Affiliations

Author notes

Article

History

Funding

Categories

Comments

Comment on this article

Similar content 378

Cited by 4

Most referenced authors 1,669