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Article ; Online: Cancer-mesothelial and cancer-macrophage interactions in the ovarian cancer microenvironment.

Jazwinska, Dorota E / Kulawiec, Diana G / Zervantonakis, Ioannis K

American journal of physiology. Cell physiology

2023 Volume 325, Issue 3, Page(s) C721–C730

Abstract: The metastatic ovarian cancer microenvironment is characterized by an intricate interaction network between cancer cells and host cells. This complex heterotypic cancer-host cell crosstalk results in an environment that promotes cancer cell metastasis ... ...

Abstract	The metastatic ovarian cancer microenvironment is characterized by an intricate interaction network between cancer cells and host cells. This complex heterotypic cancer-host cell crosstalk results in an environment that promotes cancer cell metastasis and treatment resistance, leading to poor patient prognosis and survival. In this review, we focus on two host cell types found in the ovarian cancer microenvironment: mesothelial cells and tumor-associated macrophages. Mesothelial cells make up the protective lining of organs in the abdominal cavity. Cancer cells attach and invade through the mesothelial monolayer to form metastatic lesions. Crosstalk between mesothelial and cancer cells can contribute to metastatic progression and chemotherapy resistance. Tumor-associated macrophages are the most abundant immune cell type in the ovarian cancer microenvironment with heterogeneous subpopulations exhibiting protumor or antitumor functions. Macrophage reprogramming toward a protumor or antitumor state can be influenced by chemotherapy and communication with cancer cells, resulting in cancer cell invasion and treatment resistance. A better understanding of cancer-mesothelial and cancer-macrophage crosstalk will uncover biomarkers of metastatic progression and therapeutic targets to restore chemotherapy sensitivity.
MeSH term(s)	Humans ; Female ; Tumor Microenvironment ; Cell Line, Tumor ; Epithelium/metabolism ; Ovarian Neoplasms/drug therapy ; Macrophages/metabolism
Language	English
Publishing date	2023-08-07
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00461.2022
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Article ; Online: Beyond matrix stiffness: targeting force-induced cancer drug resistance.

Kalli, Maria / Poskus, Matthew D / Stylianopoulos, Triantafyllos / Zervantonakis, Ioannis K

Trends in cancer

2023 Volume 9, Issue 11, Page(s) 937–954

Abstract: During tumor progression, mechanical abnormalities in the tumor microenvironment (TME) trigger signaling pathways in cells that activate cellular programs, resulting in tumor growth and drug resistance. In this review, we describe mechanisms of action ... ...

Abstract	During tumor progression, mechanical abnormalities in the tumor microenvironment (TME) trigger signaling pathways in cells that activate cellular programs, resulting in tumor growth and drug resistance. In this review, we describe mechanisms of action for anti-cancer therapies and mechanotransduction programs that regulate cellular processes, including cell proliferation, apoptosis, survival and phenotype switching. We discuss how the therapeutic response is impacted by the three main mechanical TME abnormalities: high extracellular matrix (ECM) composition and stiffness; interstitial fluid pressure (IFP); and elevated mechanical forces. We also review drugs that normalize these abnormalities or block mechanosensors and mechanotransduction pathways. Finally, we discuss current challenges and perspectives for the development of new strategies targeting mechanically induced drug resistance in the clinic.
MeSH term(s)	Humans ; Mechanotransduction, Cellular ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Signal Transduction ; Extracellular Matrix/pathology ; Drug Resistance, Neoplasm ; Tumor Microenvironment
Language	English
Publishing date	2023-08-08
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2852626-0
ISSN	2405-8025 ; 2405-8033 ; 2405-8033
ISSN (online)	2405-8025 ; 2405-8033
ISSN	2405-8033
DOI	10.1016/j.trecan.2023.07.006
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Article ; Online: Therapy resistance: opportunities created by adaptive responses to targeted therapies in cancer.

Labrie, Marilyne / Brugge, Joan S / Mills, Gordon B / Zervantonakis, Ioannis K

Nature reviews. Cancer

2022 Volume 22, Issue 6, Page(s) 323–339

Abstract: Normal cells explore multiple states to survive stresses encountered during development and self-renewal as well as environmental stresses such as starvation, DNA damage, toxins or infection. Cancer cells co-opt normal stress mitigation pathways to ... ...

Abstract	Normal cells explore multiple states to survive stresses encountered during development and self-renewal as well as environmental stresses such as starvation, DNA damage, toxins or infection. Cancer cells co-opt normal stress mitigation pathways to survive stresses that accompany tumour initiation, progression, metastasis and immune evasion. Cancer therapies accentuate cancer cell stresses and invoke rapid non-genomic stress mitigation processes that maintain cell viability and thus represent key targetable resistance mechanisms. In this Review, we describe mechanisms by which tumour ecosystems, including cancer cells, immune cells and stroma, adapt to therapeutic stresses and describe three different approaches to exploit stress mitigation processes: (1) interdict stress mitigation to induce cell death; (2) increase stress to induce cellular catastrophe; and (3) exploit emergent vulnerabilities in cancer cells and cells of the tumour microenvironment. We review challenges associated with tumour heterogeneity, prioritizing actionable adaptive responses for optimal therapeutic outcomes, and development of an integrative framework to identify and target vulnerabilities that arise from adaptive responses and engagement of stress mitigation pathways. Finally, we discuss the need to monitor adaptive responses across multiple scales and translation of combination therapies designed to take advantage of adaptive responses and stress mitigation pathways to the clinic.
MeSH term(s)	DNA Damage ; Ecosystem ; Humans ; Immunotherapy ; Neoplasms/pathology ; Tumor Microenvironment
Language	English
Publishing date	2022-03-09
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/s41568-022-00454-5
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Zs.A 5563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: CAR T cell infiltration and cytotoxic killing within the core of 3D breast cancer spheroids under control of antigen sensing in microwell arrays.

Cho, Youngbin / Laird, Matthew / Bishop, Teddi / Li, Ruxuan / Ruffo, Elisa / Lohmueller, Jason / Zervantonakis, Ioannis K

bioRxiv : the preprint server for biology

2024

Abstract: The success of chimeric antigen receptor (CAR) T cells in blood cancers has intensified efforts to develop CAR T therapies for solid cancers. In the solid tumor microenvironment, CAR T cell trafficking and suppression of cytotoxic killing represent ... ...

Abstract	The success of chimeric antigen receptor (CAR) T cells in blood cancers has intensified efforts to develop CAR T therapies for solid cancers. In the solid tumor microenvironment, CAR T cell trafficking and suppression of cytotoxic killing represent limiting factors for therapeutic efficacy. Here, we present a microwell platform to study CAR T cell interactions with 3D tumor spheroids and determine predictors of anti-tumor CAR T cell function. To precisely control antigen sensing by CAR T cells, we utilized a switchable adaptor CAR system, that instead of directly binding to an antigen of interest, covalently attaches to co-administered antibody adaptors that mediate tumor antigen recognition. Following addition of an anti-HER2 adaptor antibody, primary human CAR T cells exhibited higher infiltration and clustering compared to the no adaptor control. By tracking CAR T cell killing at the individual spheroid level, we showed the suppressive effects of spheroid size and identified the initial CAR T cell : spheroid area ratio as a predictor of cytotoxicity. Spatiotemporal analysis revealed lower CAR T cell numbers and cytotoxicity in the spheroid core compared to the periphery. Finally, increasing CAR T cell seeding density, resulted in higher CAR T cell infiltration and cancer cell elimination in the spheroid core. Our findings provide new quantitative insights into CAR T cell-mediated killing of HER2+ breast tumor cells. Given the miniaturized nature and live imaging capabilities, our microfabricated system holds promise for discovering cell-cell interaction mechanisms that orchestrate antitumor CAR T cell functions and screening cellular immunotherapies in 3D tumor models.
Language	English
Publishing date	2024-03-15
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.14.585033
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Article ; Online: Fabrication of 3D-printed molds for polydimethylsiloxane-based microfluidic devices using a liquid crystal display-based vat photopolymerization process: printing quality, drug response and 3D invasion cell culture assays.

Poskus, Matthew D / Wang, Tuo / Deng, Yuxuan / Borcherding, Sydney / Atkinson, Jake / Zervantonakis, Ioannis K

Microsystems & nanoengineering

2023 Volume 9, Page(s) 140

Abstract: Microfluidic platforms enable more precise control of biological stimuli and environment dimensionality than conventional macroscale cell-based assays; however, long fabrication times and high-cost specialized equipment limit the widespread adoption of ... ...

Abstract	Microfluidic platforms enable more precise control of biological stimuli and environment dimensionality than conventional macroscale cell-based assays; however, long fabrication times and high-cost specialized equipment limit the widespread adoption of microfluidic technologies. Recent improvements in vat photopolymerization three-dimensional (3D) printing technologies such as liquid crystal display (LCD) printing offer rapid prototyping and a cost-effective solution to microfluidic fabrication. Limited information is available about how 3D printing parameters and resin cytocompatibility impact the performance of 3D-printed molds for the fabrication of polydimethylsiloxane (PDMS)-based microfluidic platforms for cellular studies. Using a low-cost, commercially available LCD-based 3D printer, we assessed the cytocompatibility of several resins, optimized fabrication parameters, and characterized the minimum feature size. We evaluated the response to both cytotoxic chemotherapy and targeted kinase therapies in microfluidic devices fabricated using our 3D-printed molds and demonstrated the establishment of flow-based concentration gradients. Furthermore, we monitored real-time cancer cell and fibroblast migration in a 3D matrix environment that was dependent on environmental signals. These results demonstrate how vat photopolymerization LCD-based fabrication can accelerate the prototyping of microfluidic platforms with increased accessibility and resolution for PDMS-based cell culture assays.
Language	English
Publishing date	2023-11-09
Publishing country	England
Document type	Journal Article
ISSN	2055-7434
ISSN (online)	2055-7434
DOI	10.1038/s41378-023-00607-y
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Article: Cancer-cell derived S100A11 promotes macrophage recruitment in ER+ breast cancer.

Lee, Sanghoon / Cho, Youngbin / Li, Yiting / Li, Ruxuan / Brown, Daniel / McAuliffe, Priscilla / Lee, Adrian V / Oesterreich, Steffi / Zervantonakis, Ioannis K / Osmanbeyoglu, Hatice Ulku

bioRxiv : the preprint server for biology

2024

Abstract: Macrophages are pivotal in driving breast tumor development, progression, and resistance to treatment, particularly in estrogen receptor-positive (ER+) tumors, where they infiltrate the tumor microenvironment (TME) influenced by cancer cell-secreted ... ...

Abstract	Macrophages are pivotal in driving breast tumor development, progression, and resistance to treatment, particularly in estrogen receptor-positive (ER+) tumors, where they infiltrate the tumor microenvironment (TME) influenced by cancer cell-secreted factors. By analyzing single-cell RNA-sequencing data from 25 ER+ tumors, we elucidated interactions between cancer cells and macrophages, correlating macrophage density with epithelial cancer cell density. We identified that S100A11, a previously unexplored factor in macrophage-cancer crosstalk, predicts high macrophage density and poor outcomes in ER+ tumors. We found that recombinant S100A11 enhances macrophage infiltration and migration in a dose-dependent manner. Additionally, in 3D models, we showed that S100A11 expression levels in ER+ cancer cells predict macrophage infiltration patterns. Neutralizing S100A11 decreased macrophage recruitment, both in cancer cell lines and in a clinically relevant patient-derived organoid model, underscoring its role as a paracrine regulator of cancer-macrophage interactions in the protumorigenic TME. This study offers novel insights into the interplay between macrophages and cancer cells in ER+ breast tumors, highlighting S100A11 as a potential therapeutic target to modulate the macrophage-rich tumor microenvironment.
Language	English
Publishing date	2024-03-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.21.586041
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Article ; Online: Controlled Drug Release and Chemotherapy Response in a Novel Acoustofluidic 3D Tumor Platform.

Zervantonakis, Ioannis K / Arvanitis, Costas D

Small (Weinheim an der Bergstrasse, Germany)

2016 Volume 12, Issue 19, Page(s) 2616–2626

Abstract: Overcoming transport barriers to delivery of therapeutic agents in tumors remains a major challenge. Focused ultrasound (FUS), in combination with modern nanomedicine drug formulations, offers the ability to maximize drug transport to tumor tissue while ... ...

Abstract	Overcoming transport barriers to delivery of therapeutic agents in tumors remains a major challenge. Focused ultrasound (FUS), in combination with modern nanomedicine drug formulations, offers the ability to maximize drug transport to tumor tissue while minimizing toxicity to normal tissue. This potential remains unfulfilled due to the limitations of current approaches in accurately assessing and quantifying how FUS modulates drug transport in solid tumors. A novel acoustofluidic platform is developed by integrating a physiologically relevant 3D microfluidic device and a FUS system with a closed-loop controller to study drug transport and assess the response of cancer cells to chemotherapy in real time using live cell microscopy. FUS-induced heating triggers local release of the chemotherapeutic agent doxorubicin from a liposomal carrier and results in higher cellular drug uptake in the FUS focal region. This differential drug uptake induces locally confined DNA damage and glioblastoma cell death in the 3D environment. The capabilities of acoustofluidics for accurate control of drug release and monitoring of localized cell response are demonstrated in a 3D in vitro tumor mode. This has important implications for developing novel strategies to deliver therapeutic agents directly to the tumor tissue while sparing healthy tissue.
Language	English
Publishing date	2016
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1613-6829
ISSN (online)	1613-6829
DOI	10.1002/smll.201503342
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Article ; Online: Mechanical Stress Signaling in Pancreatic Cancer Cells Triggers p38 MAPK- and JNK-Dependent Cytoskeleton Remodeling and Promotes Cell Migration via Rac1/cdc42/Myosin II.

Kalli, Maria / Li, Ruxuan / Mills, Gordon B / Stylianopoulos, Triantafyllos / Zervantonakis, Ioannis K

Molecular cancer research : MCR

2021 Volume 20, Issue 3, Page(s) 485–497

Abstract: Advanced or metastatic pancreatic cancer is highly resistant to existing therapies, and new treatments are urgently needed to improve patient outcomes. Current studies focus on alternative treatment approaches that target the abnormal microenvironment of ...

Abstract	Advanced or metastatic pancreatic cancer is highly resistant to existing therapies, and new treatments are urgently needed to improve patient outcomes. Current studies focus on alternative treatment approaches that target the abnormal microenvironment of pancreatic tumors and the resulting elevated mechanical stress in the tumor interior. Nevertheless, the underlying mechanisms by which mechanical stress regulates pancreatic cancer metastatic potential remain elusive. Herein, we used a proteomic assay to profile mechanical stress-induced signaling cascades that drive the motility of pancreatic cancer cells. Proteomic analysis, together with selective protein inhibition and siRNA treatments, revealed that mechanical stress enhances cell migration through activation of the p38 MAPK/HSP27 and JNK/c-Jun signaling axes, and activation of the actin cytoskeleton remodelers: Rac1, cdc42, and myosin II. In addition, mechanical stress upregulated transcription factors associated with epithelial-to-mesenchymal transition and stimulated the formation of stress fibers and filopodia. p38 MAPK and JNK inhibition resulted in lower cell proliferation and more effectively blocked cell migration under mechanical stress compared with control conditions. The enhanced tumor cell motility under mechanical stress was potently reduced by cdc42 and Rac1 silencing with no effects on proliferation. Our results highlight the importance of targeting aberrant signaling in cancer cells that have adapted to mechanical stress in the tumor microenvironment, as a novel approach to effectively limit pancreatic cancer cell migration. Implications: Our findings highlight that mechanical stress activated the p38 MAPK and JNK signaling axis and stimulated pancreatic cancer cell migration via upregulation of the actin cytoskeleton remodelers cdc42 and Rac1.
MeSH term(s)	Actin Cytoskeleton/metabolism ; Cell Movement ; Cytoskeletal Proteins/metabolism ; Humans ; Myosin Type II/metabolism ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Proteomics ; Stress, Mechanical ; Tumor Microenvironment ; p38 Mitogen-Activated Protein Kinases/genetics ; p38 Mitogen-Activated Protein Kinases/metabolism ; rac1 GTP-Binding Protein/genetics ; rac1 GTP-Binding Protein/metabolism
Chemical Substances	Cytoskeletal Proteins ; RAC1 protein, human ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Myosin Type II (EC 3.6.1.-) ; rac1 GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2021-11-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-21-0266
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Article ; Online: Investigating key cell types and molecules dynamics in PyMT mice model of breast cancer through a mathematical model.

Mohammad Mirzaei, Navid / Changizi, Navid / Asadpoure, Alireza / Su, Sumeyye / Sofia, Dilruba / Tatarova, Zuzana / Zervantonakis, Ioannis K / Chang, Young Hwan / Shahriyari, Leili

PLoS computational biology

2022 Volume 18, Issue 3, Page(s) e1009953

Abstract: The most common kind of cancer among women is breast cancer. Understanding the tumor microenvironment and the interactions between individual cells and cytokines assists us in arriving at more effective treatments. Here, we develop a data-driven ... ...

Abstract	The most common kind of cancer among women is breast cancer. Understanding the tumor microenvironment and the interactions between individual cells and cytokines assists us in arriving at more effective treatments. Here, we develop a data-driven mathematical model to investigate the dynamics of key cell types and cytokines involved in breast cancer development. We use time-course gene expression profiles of a mouse model to estimate the relative abundance of cells and cytokines. We then employ a least-squares optimization method to evaluate the model's parameters based on the mice data. The resulting dynamics of the cells and cytokines obtained from the optimal set of parameters exhibit a decent agreement between the data and predictions. We perform a sensitivity analysis to identify the crucial parameters of the model and then perform a local bifurcation on them. The results reveal a strong connection between adipocytes, IL6, and the cancer population, suggesting them as potential targets for therapies.
MeSH term(s)	Animals ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Cytokines ; Disease Models, Animal ; Female ; Humans ; Mice ; Tumor Microenvironment
Chemical Substances	Cytokines
Language	English
Publishing date	2022-03-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2193340-6
ISSN	1553-7358 ; 1553-734X
ISSN (online)	1553-7358
ISSN	1553-734X
DOI	10.1371/journal.pcbi.1009953
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Article: A PDE Model of Breast Tumor Progression in MMTV-PyMT Mice.

Mohammad Mirzaei, Navid / Tatarova, Zuzana / Hao, Wenrui / Changizi, Navid / Asadpoure, Alireza / Zervantonakis, Ioannis K / Hu, Yu / Chang, Young Hwan / Shahriyari, Leili

Journal of personalized medicine

2022 Volume 12, Issue 5

Abstract: The evolution of breast tumors greatly depends on the interaction network among different cell types, including immune cells and cancer cells in the tumor. This study takes advantage of newly collected rich spatio-temporal mouse data to develop a data- ... ...

Abstract	The evolution of breast tumors greatly depends on the interaction network among different cell types, including immune cells and cancer cells in the tumor. This study takes advantage of newly collected rich spatio-temporal mouse data to develop a data-driven mathematical model of breast tumors that considers cells' location and key interactions in the tumor. The results show that cancer cells have a minor presence in the area with the most overall immune cells, and the number of activated immune cells in the tumor is depleted over time when there is no influx of immune cells. Interestingly, in the case of the influx of immune cells, the highest concentrations of both T cells and cancer cells are in the boundary of the tumor, as we use the Robin boundary condition to model the influx of immune cells. In other words, the influx of immune cells causes a dominant outward advection for cancer cells. We also investigate the effect of cells' diffusion and immune cells' influx rates in the dynamics of cells in the tumor micro-environment. Sensitivity analyses indicate that cancer cells and adipocytes' diffusion rates are the most sensitive parameters, followed by influx and diffusion rates of cytotoxic T cells, implying that targeting them is a possible treatment strategy for breast cancer.
Language	English
Publishing date	2022-05-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662248-8
ISSN	2075-4426
ISSN	2075-4426
DOI	10.3390/jpm12050807
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