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Article ; Online: Uptake of tumor-derived microparticles induces metabolic reprogramming of macrophages in the early metastatic lung

Kelly Kersten / Ran You / Sophia Liang / Kevin M. Tharp / Joshua Pollack / Valerie M. Weaver / Matthew F. Krummel / Mark B. Headley

Cell Reports, Vol 42, Iss 6, Pp 112582- (2023)

2023

Abstract: Summary: Pre-metastatic niche formation is a critical step during the metastatic spread of cancer. One way by which primary tumors prime host cells at future metastatic sites is through the shedding of tumor-derived microparticles as a consequence of ... ...

Abstract	Summary: Pre-metastatic niche formation is a critical step during the metastatic spread of cancer. One way by which primary tumors prime host cells at future metastatic sites is through the shedding of tumor-derived microparticles as a consequence of vascular sheer flow. However, it remains unclear how the uptake of such particles by resident immune cells affects their phenotype and function. Here, we show that ingestion of tumor-derived microparticles by macrophages induces a rapid metabolic and phenotypic switch that is characterized by enhanced mitochondrial mass and function, increased oxidative phosphorylation, and upregulation of adhesion molecules, resulting in reduced motility in the early metastatic lung. This reprogramming event is dependent on signaling through the mTORC1, but not the mTORC2, pathway and is induced by uptake of tumor-derived microparticles. Together, these data support a mechanism by which uptake of tumor-derived microparticles induces reprogramming of macrophages to shape their fate and function in the early metastatic lung.
Keywords	CP: Cancer ; CP: Metabolism ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2023-06-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Proteoglycans as Mediators of Cancer Tissue Mechanics

Anna Barkovskaya / Alexander Buffone / Martin Žídek / Valerie M. Weaver

Frontiers in Cell and Developmental Biology, Vol

2020 Volume 8

Abstract: Proteoglycans are a diverse group of molecules which are characterized by a central protein backbone that is decorated with a variety of linear sulfated glycosaminoglycan side chains. Proteoglycans contribute significantly to the biochemical and ... ...

Abstract	Proteoglycans are a diverse group of molecules which are characterized by a central protein backbone that is decorated with a variety of linear sulfated glycosaminoglycan side chains. Proteoglycans contribute significantly to the biochemical and mechanical properties of the interstitial extracellular matrix where they modulate cellular behavior by engaging transmembrane receptors. Proteoglycans also comprise a major component of the cellular glycocalyx to influence transmembrane receptor structure/function and mechanosignaling. Through their ability to initiate biochemical and mechanosignaling in cells, proteoglycans elicit profound effects on proliferation, adhesion and migration. Pathologies including cancer and cardiovascular disease are characterized by perturbed expression of proteoglycans where they compromise cell and tissue behavior by stiffening the extracellular matrix and increasing the bulkiness of the glycocalyx. Increasing evidence indicates that a bulky glycocalyx and proteoglycan-enriched extracellular matrix promote malignant transformation, increase cancer aggression and alter anti-tumor therapy response. In this review, we focus on the contribution of proteoglycans to mechanobiology in the context of normal and transformed tissues. We discuss the significance of proteoglycans for therapy response, and the current experimental strategies that target proteoglycans to sensitize cancer cells to treatment.
Keywords	proteoglycans ; GAG ; cancer ; mechanosignaling ; glycocalyx ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2020-11-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Immunosuppressive glycoproteins associate with breast tumor fibrosis and aggression

Kevin James Metcalf / Mary-Kate Hayward / Eric Berens / Alastair J. Ironside / Connor Stashko / E. Shelley Hwang / Valerie M. Weaver

Matrix Biology Plus, Vol 14, Iss , Pp 100105- (2022)

2022

Abstract: Tumors feature elevated sialoglycoprotein content. Sialoglycoproteins promote tumor progression and are linked to immune suppression via the sialic acid-Siglec axis. Understanding factors that increase sialoglycoprotein biosynthesis in tumors could ... ...

Abstract	Tumors feature elevated sialoglycoprotein content. Sialoglycoproteins promote tumor progression and are linked to immune suppression via the sialic acid-Siglec axis. Understanding factors that increase sialoglycoprotein biosynthesis in tumors could identify approaches to improve patient response to immunotherapy. We quantified higher levels of sialoglycoproteins in the fibrotic regions within human breast tumor tissues. Human breast tumor subtypes, which are more fibrotic, similarly featured increased sialoglycoprotein content. Further analysis revealed the breast cancer cells as the primary cell type synthesizing and secreting the tumor tissue sialoglycoproteins and confirmed that the more aggressive, fibrotic breast cancer subtypes expressed the highest levels of sialoglycoprotein biosynthetic genes. The more aggressive breast cancer subtypes also featured greater infiltration of immunosuppressive SIGLEC7, SIGLEC9, and SIGLEC10-pos myeloid cells, indicating that triple-negative breast tumors had higher expression of both immunosuppressive Siglec receptors and their cognate ligands. The findings link sialoglycoprotein biosynthesis and secretion to tumor fibrosis and aggression in human breast tumors. The data suggest targeting of the sialic acid-Siglec axis may comprise an attractive therapeutic target particularly for the more aggressive HER2+ and triple-negative breast cancer subtypes.
Keywords	Sialic acid ; Sialoglycoproteins ; Siglec receptors ; Breast cancer ; Fibrosis ; Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: NCI's publication affiliation conundrum

Susan Samson / Jason J. Northey / Irene Acerbi / Andrei Goga / Carl L. Flink / Valerie M. Weaver / Mark A. LaBarge

Translational Oncology, Vol 16, Iss , Pp 101325- (2022)

Reframing innovation to incentivize an equitable path for advocate representation

2022

Abstract: Advocacy engagement has been at the forefront of National Cancer Institute (NCI) efforts to advance scientific discoveries and transform medical interventions. Nonetheless, the journey for advocates has been uneven. Case in Point: NCI publication ... ...

Abstract	Advocacy engagement has been at the forefront of National Cancer Institute (NCI) efforts to advance scientific discoveries and transform medical interventions. Nonetheless, the journey for advocates has been uneven. Case in Point: NCI publication affiliation rules of engagement pose unique equity challenges while raising questions about structural representation in biomedical research. Abiding by the core rationale that publication affiliation should be tailored to employment status, the NCI has systematically denied research advocate volunteers the opportunity to specifically list NCI as an institutional affiliation on academic publications. Unpacking advocate NCI publication affiliation restrictions and its links with advocacy heritage preservation and convergent science goals poses unique diversity, equity, and inclusion challenges and opportunities. Improving the quality of structural representation in biomedical research requires new theories of action and flexible planning to advance, promote and build capacity for strategic advocacy inclusion and equity within publication affiliation initiatives. Here we highlight several opportunities for how leadership might formulate a radically different vision for NCI's approach. This perspective interrogates the best way forward for ensuring that biomedical employee and volunteer advocate workforce publication affiliation intersections are characterized by increased creativity and representation parity. Imbuing the scientist and clinical researcher archetype with social dimensions, we join NCI critical thinkers in urging employees, funded academics, and volunteer citizen scientists to collectively assume the role as paladins of science and integrity who view the triumphs of making a difference in science alongside the social responsibility of promoting transdisciplinary professionalism and the democratization of science.
Keywords	Convergent science ; Cancer research advocacy ; Reframing innovation ; NCI publication affiliation practices ; Diversity ; equity and inclusion (DE&I) ; Advocacy heritage preservation ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
Subject code	001
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Feeling Stress

Josette M. Northcott / Ivory S. Dean / Janna K. Mouw / Valerie M. Weaver

Frontiers in Cell and Developmental Biology, Vol

The Mechanics of Cancer Progression and Aggression

2018 Volume 6

Abstract: The tumor microenvironment is a dynamic landscape in which the physical and mechanical properties evolve dramatically throughout cancer progression. These changes are driven by enhanced tumor cell contractility and expansion of the growing tumor mass, as ...

Abstract	The tumor microenvironment is a dynamic landscape in which the physical and mechanical properties evolve dramatically throughout cancer progression. These changes are driven by enhanced tumor cell contractility and expansion of the growing tumor mass, as well as through alterations to the material properties of the surrounding extracellular matrix (ECM). Consequently, tumor cells are exposed to a number of different mechanical inputs including cell–cell and cell-ECM tension, compression stress, interstitial fluid pressure and shear stress. Oncogenes engage signaling pathways that are activated in response to mechanical stress, thereby reworking the cell's intrinsic response to exogenous mechanical stimuli, enhancing intracellular tension via elevated actomyosin contraction, and influencing ECM stiffness and tissue morphology. In addition to altering their intracellular tension and remodeling the microenvironment, cells actively respond to these mechanical perturbations phenotypically through modification of gene expression. Herein, we present a description of the physical changes that promote tumor progression and aggression, discuss their interrelationship and highlight emerging therapeutic strategies to alleviate the mechanical stresses driving cancer to malignancy.
Keywords	cancer progression ; cell contractility ; mechanical stresses ; tissue tension ; solid stress ; ECM stiffness ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2018-02-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: A 3D tension bioreactor platform to study the interplay between ECM stiffness and tumor phenotype

Cassereau, Luke / Guanqing Ou / Johnathon Lakins / Valerie M. Weaver / Yekaterina A. Miroshnikova

Journal of biotechnology. 2015 Jan. 10, v. 193

2015

Abstract: Extracellular matrix (ECM) structure, composition, and stiffness have profound effects on tissue development and pathologies such as cardiovascular disease and cancer. Accordingly, a variety of synthetic hydrogel systems have been designed to study the ... ...

Abstract	Extracellular matrix (ECM) structure, composition, and stiffness have profound effects on tissue development and pathologies such as cardiovascular disease and cancer. Accordingly, a variety of synthetic hydrogel systems have been designed to study the impact of ECM composition, density, mechanics, and topography on cell and tissue phenotype. However, these synthetic systems fail to accurately recapitulate the biological properties and structure of the native tissue ECM. Natural three dimensional (3D) ECM hydrogels, such as collagen or hyaluronic acid, feature many of the chemical and physical properties of tissue, yet, these systems have limitations including the inability to independently control biophysical properties such as stiffness and pore size. Here, we present a 3D tension bioreactor system that permits precise mechanical tuning of collagen hydrogel stiffness, while maintaining consistent composition and pore size. We achieve this by mechanically loading collagen hydrogels covalently-conjugated to a polydimethylsiloxane (PDMS) membrane to induce hydrogel stiffening. We validated the biological application of this system with oncogenically transformed mammary epithelial cell organoids embedded in a 3D collagen I hydrogel, either uniformly stiffened or calibrated to create a gradient of ECM stiffening, to visually demonstrate the impact of ECM stiffening on transformation and tumor cell invasion. As such, this bioreactor presents the first tunable 3D natural hydrogel system that is capable of independently assessing the role of ECM stiffness on tissue phenotype.
Keywords	bioreactors ; cardiovascular diseases ; cell invasion ; collagen ; epithelial cells ; extracellular matrix ; hyaluronic acid ; hydrocolloids ; mammary glands ; mechanics ; neoplasm cells ; neoplasms ; phenotype ; porosity ; topography
Language	English
Dates of publication	2015-0110
Size	p. 66-69.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	843647-2
ISSN	1873-4863 ; 0168-1656 ; 1389-0352
ISSN (online)	1873-4863
ISSN	0168-1656 ; 1389-0352
DOI	10.1016/j.jbiotec.2014.11.008
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Single-cell transcriptome analysis defines heterogeneity of the murine pancreatic ductal tree

eLife, Vol

2021 Volume 10

Abstract: To study disease development, an inventory of an organ's cell types and understanding of physiologic function is paramount. Here, we performed single-cell RNA-sequencing to examine heterogeneity of murine pancreatic duct cells, pancreatobiliary cells, ... ...

Abstract	To study disease development, an inventory of an organ's cell types and understanding of physiologic function is paramount. Here, we performed single-cell RNA-sequencing to examine heterogeneity of murine pancreatic duct cells, pancreatobiliary cells, and intrapancreatic bile duct cells. We describe an epithelial-mesenchymal transitory axis in our three pancreatic duct subpopulations and identify osteopontin as a regulator of this fate decision as well as human duct cell dedifferentiation. Our results further identify functional heterogeneity within pancreatic duct subpopulations by elucidating a role for geminin in accumulation of DNA damage in the setting of chronic pancreatitis. Our findings implicate diverse functional roles for subpopulations of pancreatic duct cells in maintenance of duct cell identity and disease progression and establish a comprehensive road map of murine pancreatic duct cell, pancreatobiliary cell, and intrapancreatic bile duct cell homeostasis.
Keywords	scRNA-seq ; pancreatic duct ligation ; Osteopontin ; Geminin ; duct heterogeneity ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-05-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Spatiotemporal mosaic self-patterning of pluripotent stem cells using CRISPR interference

Ashley RG Libby / David A Joy / Po-Lin So / Mohammad A Mandegar / Jonathon M Muncie / Federico N Mendoza-Camacho / Valerie M Weaver / Bruce R Conklin / Todd C McDevitt

eLife, Vol

2018 Volume 7

Abstract: Morphogenesis involves interactions of asymmetric cell populations to form complex multicellular patterns and structures comprised of distinct cell types. However, current methods to model morphogenic events lack control over cell-type co-emergence and ... ...

Abstract	Morphogenesis involves interactions of asymmetric cell populations to form complex multicellular patterns and structures comprised of distinct cell types. However, current methods to model morphogenic events lack control over cell-type co-emergence and offer little capability to selectively perturb specific cell subpopulations. Our in vitro system interrogates cell-cell interactions and multicellular organization within human induced pluripotent stem cell (hiPSC) colonies. We examined effects of induced mosaic knockdown of molecular regulators of cortical tension (ROCK1) and cell-cell adhesion (CDH1) with CRISPR interference. Mosaic knockdown of ROCK1 or CDH1 resulted in differential patterning within hiPSC colonies due to cellular self-organization, while retaining an epithelial pluripotent phenotype. Knockdown induction stimulates a transient wave of differential gene expression within the mixed populations that stabilized in coordination with observed self-organization. Mosaic patterning enables genetic interrogation of emergent multicellular properties, which can facilitate better understanding of the molecular pathways that regulate symmetry-breaking during morphogenesis.
Keywords	pluripotent stem cells ; morphogenesis ; bio-engineering ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2018-10-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Comprehensive characterization of DNA methylation changes in Fuchs endothelial corneal dystrophy.

Emily Khuc / Russell Bainer / Marie Wolf / Selene M Clay / Daniel J Weisenberger / Jacquelyn Kemmer / Valerie M Weaver / David G Hwang / Matilda F Chan

PLoS ONE, Vol 12, Iss 4, p e

2017 Volume 0175112

Abstract: Transparency of the human cornea is necessary for vision. Fuchs Endothelial Corneal Dystrophy (FECD) is a bilateral, heritable degeneration of the corneal endothelium, and a leading indication for corneal transplantation in developed countries. While the ...

Abstract	Transparency of the human cornea is necessary for vision. Fuchs Endothelial Corneal Dystrophy (FECD) is a bilateral, heritable degeneration of the corneal endothelium, and a leading indication for corneal transplantation in developed countries. While the early onset, and rarer, form of FECD has been linked to COL8A2 mutations, the more common, late onset form of FECD has genetic mutations linked to only a minority of cases. Epigenetic modifications that occur in FECD are unknown. Here, we report on and compare the DNA methylation landscape of normal human corneal endothelial (CE) tissue and CE from FECD patients using the Illumina Infinium HumanMethylation450 (HM450) DNA methylation array. We show that DNA methylation profiles are distinct between control and FECD samples. Differentially methylated probes (10,961) were identified in the FECD samples compared with the control samples, with the majority of probes being hypermethylated in the FECD samples. Genes containing differentially methylated sites were disproportionately annotated to ontological categories involving cytoskeletal organization, ion transport, hematopoetic cell differentiation, and cellular metabolism. Our results suggest that altered DNA methylation patterns may contribute to loss of corneal transparency in FECD through a global accumulation of sporadic DNA methylation changes in genes critical to basic CE biological processes.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2017-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A bulky glycocalyx fosters metastasis formation by promoting G1 cell cycle progression

Elliot C Woods / FuiBoon Kai / J Matthew Barnes / Kayvon Pedram / Michael W Pickup / Michael J Hollander / Valerie M Weaver / Carolyn R Bertozzi

eLife, Vol

2017 Volume 6

Abstract: Metastasis depends upon cancer cell growth and survival within the metastatic niche. Tumors which remodel their glycocalyces, by overexpressing bulky glycoproteins like mucins, exhibit a higher predisposition to metastasize, but the role of mucins in ... ...

Abstract	Metastasis depends upon cancer cell growth and survival within the metastatic niche. Tumors which remodel their glycocalyces, by overexpressing bulky glycoproteins like mucins, exhibit a higher predisposition to metastasize, but the role of mucins in oncogenesis remains poorly understood. Here we report that a bulky glycocalyx promotes the expansion of disseminated tumor cells in vivo by fostering integrin adhesion assembly to permit G1 cell cycle progression. We engineered tumor cells to display glycocalyces of various thicknesses by coating them with synthetic mucin-mimetic glycopolymers. Cells adorned with longer glycopolymers showed increased metastatic potential, enhanced cell cycle progression, and greater levels of integrin-FAK mechanosignaling and Akt signaling in a syngeneic mouse model of metastasis. These effects were mirrored by expression of the ectodomain of cancer-associated mucin MUC1. These findings functionally link mucinous proteins with tumor aggression, and offer a new view of the cancer glycocalyx as a major driver of disease progression.
Keywords	glycocalyx ; mucins ; integrins ; metastasis ; cell proliferation ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2017-12-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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