Multifaced roles of PLAC8 in cancer

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Abstract

The role of PLAC8 in tumorigenesis has been gradually elucidated with the development of research. Although there are common molecular mechanisms that enforce cell growth, the impact of PLAC8 is varied and can, in some instances, have opposite effects on tumorigenesis. To systematically understand the role of PLAC8 in tumors, the molecular functions of PLAC8 in cancer will be discussed by focusing on how PLAC8 impacts tumorigenesis when it arises within tumor cells and how these roles can change in different stages of cancer progression with the ultimate goal of suppressing PLAC8-relevant cancer behavior and related pathologies. In addition, we highlight the diversity of PLAC8 in different tumors and its functional output beyond cancer cell growth. The comprehension of PLAC8’s molecular function might provide new target and lead to the development of novel anticancer therapies.

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Ferroptosis: an iron-dependent form of nonapoptotic cell death.

Scott J. Dixon, Kathryn Lemberg, Michael Lamprecht … (2012)

Nonapoptotic forms of cell death may facilitate the selective elimination of some tumor cells or be activated in specific pathological states. The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of nonapoptotic cell death that we term ferroptosis. Ferroptosis is dependent upon intracellular iron, but not other metals, and is morphologically, biochemically, and genetically distinct from apoptosis, necrosis, and autophagy. We identify the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes. Indeed, erastin, like glutamate, inhibits cystine uptake by the cystine/glutamate antiporter (system x(c)(-)), creating a void in the antioxidant defenses of the cell and ultimately leading to iron-dependent, oxidative death. Thus, activation of ferroptosis results in the nonapoptotic destruction of certain cancer cells, whereas inhibition of this process may protect organisms from neurodegeneration. Copyright © 2012 Elsevier Inc. All rights reserved.

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EMT Transition States during Tumor Progression and Metastasis

Ievgenia Pastushenko, Cédric Blanpain (2018)

Epithelial-mesenchymal transition (EMT) is a process in which epithelial cells acquire mesenchymal features. In cancer, EMT is associated with tumor initiation, invasion, metastasis, and resistance to therapy. Recently, it has been demonstrated that EMT is not a binary process, but occurs through distinct cellular states. Here, we review the recent studies that demonstrate the existence of these different EMT states in cancer and the mechanisms regulating their functions. We discuss the different functional characteristics, such as proliferation, propagation, plasticity, invasion, and metastasis associated with the distinct EMT states. We summarize the role of the transcriptional and epigenetic landscapes, gene regulatory network and their surrounding niche in controlling the transition through the different EMT states.

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The molecular machinery of regulated cell death

Daolin Tang, Rui Kang, Tom Vanden Berghe … (2019)

Cells may die from accidental cell death (ACD) or regulated cell death (RCD). ACD is a biologically uncontrolled process, whereas RCD involves tightly structured signaling cascades and molecularly defined effector mechanisms. A growing number of novel non-apoptotic forms of RCD have been identified and are increasingly being implicated in various human pathologies. Here, we critically review the current state of the art regarding non-apoptotic types of RCD, including necroptosis, pyroptosis, ferroptosis, entotic cell death, netotic cell death, parthanatos, lysosome-dependent cell death, autophagy-dependent cell death, alkaliptosis and oxeiptosis. The in-depth comprehension of each of these lethal subroutines and their intercellular consequences may uncover novel therapeutic targets for the avoidance of pathogenic cell loss.

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Author and article information

Contributors

Jichun Zhou: jichun-zhou@zju.edu.cn

Linbo Wang: linbowang@zju.edu.cn

Journal

Journal ID (nlm-ta): Biomark Res

Journal ID (iso-abbrev): Biomark Res

Title: Biomarker Research

Publisher: BioMed Central (London )

ISSN (Electronic): 2050-7771

Publication date (Electronic): 9 October 2021

Publication date PMC-release: 9 October 2021

Publication date Collection: 2021

Volume: 9

Electronic Location Identifier: 73

Affiliations

[1 ]GRID grid.13402.34, ISNI 0000 0004 1759 700X, Department of Surgical Oncology, Sir Run Run Shaw Hospital, , Zhejiang University, ; Zhejiang, 310000 Hangzhou China

[2 ]Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Zhejiang, 310000 Hangzhou China

[3 ]GRID grid.469636.8, Department of Gastrointestinal Surgery, , Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, ; Taizhou, Zhejiang, 318000 People’s Republic of China

Article

Publisher ID: 329

DOI: 10.1186/s40364-021-00329-1

PMC ID: 8501656

PubMed ID: 34627411

SO-VID: 6cc1dcd3-3da7-4414-aaaa-72509a55a72a

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 26 July 2021

Date accepted : 20 September 2021

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001809, national natural science foundation of china;

Award ID: 81972453,81972597,81602471,81672729

Award Recipient : Linbo Wang

Funded by: FundRef http://dx.doi.org/10.13039/501100004731, natural science foundation of zhejiang province;

Award ID: LY19H160055, LY19H160059, LY18H160005, and LY20H160026

Award Recipient : Jichun Zhou

Funded by: FundRef http://dx.doi.org/10.13039/501100011440, zhejiang provincial key laboratory of wood science and technology;

Award ID: 2021RC016

Award Recipient : Jichun Zhou

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Keywords: plac8,tumorigenesis,cancer stemness,programmed cancer death

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Keywords: plac8, tumorigenesis, cancer stemness, programmed cancer death

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Multifaced roles of PLAC8 in cancer

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Cancer Metabolism

Most cited references 106

Ferroptosis: an iron-dependent form of nonapoptotic cell death.

EMT Transition States during Tumor Progression and Metastasis

The molecular machinery of regulated cell death

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