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Article ; Online: BNIP3 and Nix: Atypical regulators of cell fate.

Field, Jared T / Gordon, Joseph W

Biochimica et biophysica acta. Molecular cell research

2022 Volume 1869, Issue 10, Page(s) 119325

Abstract: Since their discovery nearly 25 years ago, the BCL-2 family members BNIP3 and BNIP3L (aka Nix) have been labelled 'atypical'. Originally, this was because BNIP3 and Nix have divergent BH3 domains compared to other BCL-2 proteins. In addition, this ... ...

Abstract	Since their discovery nearly 25 years ago, the BCL-2 family members BNIP3 and BNIP3L (aka Nix) have been labelled 'atypical'. Originally, this was because BNIP3 and Nix have divergent BH3 domains compared to other BCL-2 proteins. In addition, this atypical BH3 domain is dispensable for inducing cell death, which is also unusual for a 'death gene'. Instead, BNIP3 and Nix utilize a transmembrane domain, which allows for dimerization and insertion into and through organelle membranes to elicit cell death. Much has been learned regarding the biological function of these two atypical death genes, including their role in metabolic stress, where BNIP3 is responsive to hypoxia, while Nix responds variably to hypoxia and is also down-stream of PKC signaling and lipotoxic stress. Interestingly, both BNIP3 and Nix respond to signals related to cell atrophy. In addition, our current view of regulated cell death has expanded to include forms of necrosis such as necroptosis, pyroptosis, ferroptosis, and permeability transition-mediated cell death where BNIP3 and Nix have been shown to play context- and cell-type specific roles. Perhaps the most intriguing discoveries in recent years are the results demonstrating roles for BNIP3 and Nix outside of the purview of death genes, such as regulation of proliferation, differentiation/maturation, mitochondrial dynamics, macro- and selective-autophagy. We provide a historical and unbiased overview of these 'death genes', including new information related to alternative splicing and post-translational modification. In addition, we propose to redefine these two atypical members of the BCL-2 family as versatile regulators of cell fate.
MeSH term(s)	Autophagy/genetics ; Humans ; Hypoxia ; Membrane Proteins/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2 ; Tumor Suppressor Proteins/metabolism
Chemical Substances	BNIP3 protein, human ; BNIP3L protein, human ; Membrane Proteins ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2 ; Tumor Suppressor Proteins
Language	English
Publishing date	2022-07-19
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2022.119325
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Article ; Online: Regulation of cardiac myocyte cell death and differentiation by myocardin.

Gordon, Joseph W

Molecular and cellular biochemistry

2018 Volume 437, Issue 1-2, Page(s) 119–131

Abstract: Myocardin is a cardiac- and smooth muscle-enriched transcriptional co-activator that was originally described as an interacting partner of the serum response factor. Shortly after myocardin's discovery, a wealth of published literature described the role ...

Abstract	Myocardin is a cardiac- and smooth muscle-enriched transcriptional co-activator that was originally described as an interacting partner of the serum response factor. Shortly after myocardin's discovery, a wealth of published literature described the role of myocardin as a regulator of smooth muscle differentiation and phenotype modulation, while gene-targeting studies confirmed the essential role of myocardin in vascular development. More recently, myocardin has been implicated as an important regulator of cardiac myocyte differentiation in studies demonstrating direct programming of fibroblasts towards the cardiac lineage. This function of myocardin has been attributed to its physical interaction with cardiac-enriched transcription factors such as MEF2C, GATA4, and TBX5. Moreover, conditional knockout models have revealed a critical role for myocardin during cardiac chamber maturation, and a surprising function for myocardin in the regulation of cardiomyocyte proliferation, cell death, and possibly mitochondrial function. This review summarizes the literature surrounding the cardiac-specific roles of myocardin during development and post-natal cardiac remodeling. In addition, we take a bioinformatics and computational approach to discuss known and predicted interactions and biological functions of myocardin, which suggests areas for future research.
MeSH term(s)	Animals ; Cell Death ; Cell Differentiation/physiology ; Cell Proliferation/physiology ; Fibroblasts/cytology ; Fibroblasts/metabolism ; Humans ; Mitochondria, Heart/metabolism ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/metabolism ; Nuclear Proteins/metabolism ; Trans-Activators/metabolism ; Transcription Factors/metabolism
Chemical Substances	Nuclear Proteins ; Trans-Activators ; Transcription Factors ; myocardin
Language	English
Publishing date	2018-01
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	184833-1
ISSN	1573-4919 ; 0300-8177
ISSN (online)	1573-4919
ISSN	0300-8177
DOI	10.1007/s11010-017-3100-3
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Article ; Online: Transforming Growth Factor Beta and Alveolar Rhabdomyosarcoma: A Challenge of Tumor Differentiation and Chemotherapy Response.

Bhushan, Bhavya / Iranpour, Rosa / Eshtiaghi, Amirmohammad / da Silva Rosa, Simone C / Lindsey, Benjamin W / Gordon, Joseph W / Ghavami, Saeid

International journal of molecular sciences

2024 Volume 25, Issue 5

Abstract: Alveolar rhabdomyosarcoma (ARMS), an invasive subtype of rhabdomyosarcoma (RMS), is associated with chromosomal translocation events resulting in one of two oncogenic fusion genes, ...

Abstract	Alveolar rhabdomyosarcoma (ARMS), an invasive subtype of rhabdomyosarcoma (RMS), is associated with chromosomal translocation events resulting in one of two oncogenic fusion genes,
MeSH term(s)	Humans ; Rhabdomyosarcoma, Alveolar/genetics ; Rhabdomyosarcoma, Alveolar/metabolism ; Rhabdomyosarcoma, Alveolar/pathology ; Transforming Growth Factor beta ; Transforming Growth Factor beta1 ; Paired Box Transcription Factors/genetics ; Epithelial-Mesenchymal Transition ; Rhabdomyosarcoma/genetics ; Oncogene Proteins, Fusion/genetics
Chemical Substances	Transforming Growth Factor beta ; Transforming Growth Factor beta1 ; Paired Box Transcription Factors ; Oncogene Proteins, Fusion
Language	English
Publishing date	2024-02-28
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/ijms25052791
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Article ; Online: A new trick for an old dog? Myocardial-specific roles for prostaglandins as mediators of ischemic injury and repair.

Martens, Matthew D / Fernando, Amy S / Gordon, Joseph W

American journal of physiology. Heart and circulatory physiology

2021 Volume 320, Issue 6, Page(s) H2169–H2184

Abstract: The small lipid-derived paracrine signaling molecules known as prostaglandins have been recognized for their ability to modulate many facets of cardiovascular physiology since their initial discovery more than 85 years ago. Although the role of ... ...

Abstract	The small lipid-derived paracrine signaling molecules known as prostaglandins have been recognized for their ability to modulate many facets of cardiovascular physiology since their initial discovery more than 85 years ago. Although the role of prostaglandins in the vasculature has gained significant attention across time, a handful of historical studies have also directly implicated the cardiomyocyte in both prostaglandin synthesis and release. Recently, our understanding of how prostaglandin receptor modulation impacts and contributes to myocardial structure and function has gained attention while leaving most other components of myocardial prostaglandin metabolism and signaling unexplored. This mini-review highlights both the key historical studies that underpin modern prostaglandin research in the heart, while concurrently presenting the latest findings related to how prostaglandin metabolism and signaling impact myocardial injury and repair.
MeSH term(s)	Cytochrome P-450 Enzyme System/metabolism ; Eicosanoids/metabolism ; Fibroblasts/metabolism ; Humans ; Lipoxygenase/metabolism ; Myocardial Ischemia/metabolism ; Myocardium/metabolism ; Myocytes, Cardiac/metabolism ; Paracrine Communication ; Prostaglandin-Endoperoxide Synthases/metabolism ; Prostaglandins/metabolism ; Receptors, Prostaglandin/metabolism ; Receptors, Prostaglandin E, EP3 Subtype/metabolism ; Receptors, Prostaglandin E, EP4 Subtype/metabolism ; Regeneration
Chemical Substances	Eicosanoids ; Prostaglandins ; Receptors, Prostaglandin ; Receptors, Prostaglandin E, EP3 Subtype ; Receptors, Prostaglandin E, EP4 Subtype ; Cytochrome P-450 Enzyme System (9035-51-2) ; Lipoxygenase (EC 1.13.11.12) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1)
Language	English
Publishing date	2021-04-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00872.2020
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Article ; Online: Assessment of Stiffness-Dependent Autophagosome Formation and Apoptosis in Embryonal Rhabdomyosarcoma Tumor Cells.

Sezen, Serap / Adiguzel, Sevin / Zarepour, Atefeh / Khosravi, Arezoo / Gordon, Joseph W / Ghavami, Saeid / Zarrabi, Ali

Methods in molecular biology (Clifton, N.J.)

2024

Abstract: Remodeling of the extracellular matrix (ECM) eventually causes the stiffening of tumors and changes to the microenvironment. The stiffening alters the biological processes in cancer cells due to altered signaling through cell surface receptors. Autophagy, ...

Abstract	Remodeling of the extracellular matrix (ECM) eventually causes the stiffening of tumors and changes to the microenvironment. The stiffening alters the biological processes in cancer cells due to altered signaling through cell surface receptors. Autophagy, a key catabolic process in normal and cancer cells, is thought to be involved in mechano-transduction and the level of autophagy is probably stiffness-dependent. Here, we provide a methodology to study the effect of matrix stiffness on autophagy in embryonal rhabdomyosarcoma cells. To mimic stiffness, we seeded cells on GelMA hydrogel matrices with defined stiffness and evaluated autophagy-related endpoints. We also evaluated autophagy-dependent pathways, apoptosis, and cell viability. Specifically, we utilized immunocytochemistry and confocal microscopy to track autophagosome formation through LC3 lipidation. This approach suggests that the use of GelMA hydrogels with defined stiffness represents a novel method to evaluate the role of autophagy in embryonal rhabdomyosarcoma and other cancer cells.
Language	English
Publishing date	2024-04-23
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/7651_2024_538
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Article ; Online: The obesity-autophagy-cancer axis: Mechanistic insights and therapeutic perspectives.

Behrooz, Amir Barzegar / Cordani, Marco / Fiore, Alessandra / Donadelli, Massimo / Gordon, Joseph W / Klionsky, Daniel J / Ghavami, Saeid

Seminars in cancer biology

2024 Volume 99, Page(s) 24–44

Abstract: Autophagy, a self-degradative process vital for cellular homeostasis, plays a significant role in adipose tissue metabolism and tumorigenesis. This review aims to elucidate the complex interplay between autophagy, obesity, and cancer development, with a ... ...

Abstract	Autophagy, a self-degradative process vital for cellular homeostasis, plays a significant role in adipose tissue metabolism and tumorigenesis. This review aims to elucidate the complex interplay between autophagy, obesity, and cancer development, with a specific emphasis on how obesity-driven changes affect the regulation of autophagy and subsequent implications for cancer risk. The burgeoning epidemic of obesity underscores the relevance of this research, particularly given the established links between obesity, autophagy, and various cancers. Our exploration delves into hormonal influence, notably INS (insulin) and LEP (leptin), on obesity and autophagy interactions. Further, we draw attention to the latest findings on molecular factors linking obesity to cancer, including hormonal changes, altered metabolism, and secretory autophagy. We posit that targeting autophagy modulation may offer a potent therapeutic approach for obesity-associated cancer, pointing to promising advancements in nanocarrier-based targeted therapies for autophagy modulation. However, we also recognize the challenges inherent to these approaches, particularly concerning their precision, control, and the dual roles autophagy can play in cancer. Future research directions include identifying novel biomarkers, refining targeted therapies, and harmonizing these approaches with precision medicine principles, thereby contributing to a more personalized, effective treatment paradigm for obesity-mediated cancer.
MeSH term(s)	Humans ; Obesity/complications ; Obesity/metabolism ; Adipose Tissue/metabolism ; Treatment Outcome ; Autophagy/physiology ; Neoplasms/etiology ; Neoplasms/metabolism
Language	English
Publishing date	2024-02-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2024.01.003
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Article ; Online: The molecular mosaic of regulated cell death in the cardiovascular system.

Martens, Matthew D / Karch, Jason / Gordon, Joseph W

Biochimica et biophysica acta. Molecular basis of disease

2021 Volume 1868, Issue 1, Page(s) 166297

Abstract: Cell death is now understood to be a highly regulated process that contributes to normal development and tissue homeostasis, alongside its role in the etiology of various pathological conditions. Through detailed molecular analysis, we have come to know ... ...

Abstract	Cell death is now understood to be a highly regulated process that contributes to normal development and tissue homeostasis, alongside its role in the etiology of various pathological conditions. Through detailed molecular analysis, we have come to know that all cells do not always die in the same way, and that there are at least 7 processes involved, including: apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, and autophagy-mediated cell death. These processes act as pieces in the mosaic of cardiomyocyte cell death, which come together depending on context and stimulus. This review details each individual process, as well as highlights how they come together to produce various cardiac pathologies. By knowing how the pieces go together we can aim towards the development of efficacious therapeutics, which will enable us to prevent cardiomyocyte loss in the face of stress, both reducing mortality and improving quality of life.
MeSH term(s)	Autophagy/genetics ; Cardiovascular System/metabolism ; Cardiovascular System/pathology ; Cell Death/genetics ; Ferroptosis/genetics ; Homeostasis/genetics ; Humans ; Mitochondrial Transmembrane Permeability-Driven Necrosis/genetics ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Necroptosis/genetics ; Necrosis/genetics ; Parthanatos/genetics ; Pyroptosis/genetics
Language	English
Publishing date	2021-10-27
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2021.166297
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Article: Characterizing Extracellular Vesicles and Particles Derived from Skeletal Muscle Myoblasts and Myotubes and the Effect of Acute Contractile Activity.

Bydak, Benjamin / Pierdoná, Taiana M / Seif, Samira / Sidhom, Karim / Obi, Patience O / Labouta, Hagar I / Gordon, Joseph W / Saleem, Ayesha

Membranes

2022 Volume 12, Issue 5

Abstract: Extracellular vesicles (EVs), released from all cells, are essential to cellular communication and contain biomolecular cargo that can affect recipient cell function. Studies on the effects of contractile activity (exercise) on EVs usually rely on plasma/ ...

Abstract	Extracellular vesicles (EVs), released from all cells, are essential to cellular communication and contain biomolecular cargo that can affect recipient cell function. Studies on the effects of contractile activity (exercise) on EVs usually rely on plasma/serum-based assessments, which contain EVs from many different cells. To specifically characterize skeletal muscle−derived vesicles and the effect of acute contractile activity, we used an in vitro model where C2C12 mouse myoblasts were differentiated to form myotubes. EVs were isolated from conditioned media from muscle cells at pre-differentiation (myoblasts) and post-differentiation (myotubes) and also from acutely stimulated myotubes (1 h @ 14 V, C-Pace EM, IonOptix, Westwood, MA, USA) using total exosome isolation reagent (TEI, ThermoFisher (Waltham, MA, USA), referred to as extracellular particles [EPs]) and differential ultracentrifugation (dUC; EVs). Myotube-EPs (~98 nm) were 41% smaller than myoblast-EPs (~167 nm, p < 0.001, n = 8−10). Two-way ANOVA showed a significant main effect for the size distribution of myotube vs. myoblast-EPs (p < 0.01, n = 10−13). In comparison, myoblast-EPs displayed a bimodal size distribution profile with peaks at <200 nm and 400−600, whereas myotube-Eps were largely 50−300 nm in size. Total protein yield from myotube-EPs was nearly 15-fold higher than from the myoblast-EPs, (p < 0.001 n = 6−9). Similar biophysical characteristics were observed when EVs were isolated using dUC: myotube-EVs (~195 nm) remained 41% smaller in average size than myoblast-EVs (~330 nm, p = 0.07, n = 4−6) and had comparable size distribution profiles to EPs isolated via TEI. Myotube-EVs also had 4.7-fold higher protein yield vs. myoblast EVs (p < 0.05, n = 4−6). Myotube-EPs exhibited significantly decreased expression of exosomal marker proteins TSG101, CD63, ALIX and CD81 compared with myoblast-EPs (p < 0.05, n = 7−12). Conversely, microvesicle marker ARF6 and lipoprotein marker APO-A1 were only found in the myotube-EPs (p < 0.05, n = 4−12). There was no effect of acute stimulation on myotube-EP biophysical characteristics (n = 7) or on the expression of TSG101, ARF6 or CD81 (n = 5−6). Myoblasts treated with control or acute stimulation−derived EPs (13 µg/well) for 48 h and 72 h showed no changes in mitochondrial mass (MitoTracker Red, ThermoFisher, Waltham, MA, USA), cell viability or cell count (n = 3−4). Myoblasts treated with EP-depleted media (72 h) exhibited ~90% lower cell counts (p < 0.01, n = 3). Our data show that EVs differed in size, distribution, protein yield and expression of subtype markers pre vs. post skeletal muscle−differentiation into myotubes. There was no effect of acute stimulation on biophysical profile or protein markers in EPs. Acute stimulation−derived EPs did not alter mitochondrial mass or cell count/viability. Further investigation into the effects of chronic contractile activity on the biophysical characteristics and cargo of skeletal muscle−specific EVs are warranted.
Language	English
Publishing date	2022-04-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2614641-1
ISSN	2077-0375
ISSN	2077-0375
DOI	10.3390/membranes12050464
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Article ; Online: Mechanisms of muscle insulin resistance and the cross-talk with liver and adipose tissue.

da Silva Rosa, Simone C / Nayak, Nichole / Caymo, Andrei Miguel / Gordon, Joseph W

Physiological reports

2020 Volume 8, Issue 19, Page(s) e14607

Abstract: Insulin resistance is a metabolic disorder affecting multiple tissues and is a precursor event to type 2 diabetes (T2D). As T2D affects over 425 million people globally, there is an imperative need for research into insulin resistance to better ... ...

Abstract	Insulin resistance is a metabolic disorder affecting multiple tissues and is a precursor event to type 2 diabetes (T2D). As T2D affects over 425 million people globally, there is an imperative need for research into insulin resistance to better understand the underlying mechanisms. The proposed mechanisms involved in insulin resistance include both whole body aspects, such as inflammation and metabolic inflexibility; as well as cellular phenomena, such as lipotoxicity, ER stress, and mitochondrial dysfunction. Despite numerous studies emphasizing the role of lipotoxicity in the pathogenesis of insulin resistance, an understanding of the interplay between tissues and these proposed mechanisms is still emerging. Furthermore, the tissue-specific and unique responses each of the three major insulin target tissues and how each interconnect to regulate the whole body insulin response has become a new priority in metabolic research. With an emphasis on skeletal muscle, this mini-review highlights key similarities and differences in insulin signaling and resistance between different target-tissues, and presents the latest findings related to how these tissues communicate to control whole body metabolism.
MeSH term(s)	Adipose Tissue/metabolism ; Animals ; Humans ; Insulin/metabolism ; Insulin Resistance/physiology ; Lipid Metabolism/physiology ; Liver/metabolism ; Muscle, Skeletal/metabolism
Chemical Substances	Insulin
Language	English
Publishing date	2020-10-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.14607
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Article ; Online: A bioengineering method for modeling alveolar Rhabdomyosarcoma and assessing chemotherapy responses

Stefanek, Evan / Samiei, Ehsan / Kavoosi, Mahboubeh / Esmaeillou, Mohammad / Roustai Geraylow, Kiarash / Emami, Arya / Ashrafizadeh, Milad / Perrin, David / Gordon, Joseph W / Akbari, Mohsen / Ghavami, Saeid

MethodsX. 2021, v. 8 p.101473-

2021

Abstract: Rhabdomyosarcoma (RMS) is the most common pediatric soft-tissue malignant tumor. Treatment of RMS usually includes primary tumor resection along with systemic chemotherapy. Two-dimensional (2D) cell culture systems and animal models have been extensively ...

Abstract	Rhabdomyosarcoma (RMS) is the most common pediatric soft-tissue malignant tumor. Treatment of RMS usually includes primary tumor resection along with systemic chemotherapy. Two-dimensional (2D) cell culture systems and animal models have been extensively used for investigating the potential efficacy of new RMS treatments. However, RMS cells behave differently in 2D culture than in vivo, which has recently inspired the adoption of three-dimensional (3D) culture environments. In the current paper, we will describe the detailed methodology we have developed for fabricating a 3D engineered model to study alveolar RMS (ARMS) in vitro. This model consists of a thermally cross-linked collagen disk laden with RMS cells that mimics the structural and bio-chemical aspects of the tumor extracellular matrix (ECM). This process is highly reproducible and produces a 3D engineered model that can be used to analyze the cytotoxicity and autophagy induction of drugs on ARMS cells. The most improtant bullet points are as following:•We fabricated 3D model of ARMS.•The current ARMS 3D model can be used for screening of chemotherapy drugs.•We developed methods to detect apoptosis and autophagy in ARMS 3D model to detect the mechansims of chemotherapy agents.
Keywords	animals ; apoptosis ; autophagy ; cell culture ; collagen ; crosslinking ; cytotoxicity ; drug therapy ; extracellular matrix ; models ; neoplasms ; resection ; Alveolar Rhabdomyosarcoma 3D model ; Biofabrication ; Rhabdomyosarcoma ; Cell death ; AKT ; BSA ; DAPI ; dECM ; DNA ; DFS ; DMEM ; EM ; EthD-1 ; EDTA ; ECM ; FBS ; FOXO1 ; HEPES ; IgG ; ICC ; LC3 ; MEK ; MYOD1 ; PAX ; PDMS ; PNIPAAm ; RGD ; RMS ; RT ; RPMI ; TMZ ; 3D ; 2D
Language	English
Publishing place	Elsevier B.V.
Document type	Article ; Online
ZDB-ID	2830212-6
ISSN	2215-0161
ISSN	2215-0161
DOI	10.1016/j.mex.2021.101473
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