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Article: Insidious communication amongst cancer cells.

Rodvold, Jeffrey J / Zanetti, Maurizio

Molecular & cellular oncology

2018 Volume 5, Issue 3, Page(s) e1356898

Abstract: The tumor microenvironment is home to various types of cognate and non-cognate cell interactions. Here we comment on a newly discovered form of intercellular communication, which is based on endoplasmic reticulum stress signaling. Through this mechanism ... ...

Abstract	The tumor microenvironment is home to various types of cognate and non-cognate cell interactions. Here we comment on a newly discovered form of intercellular communication, which is based on endoplasmic reticulum stress signaling. Through this mechanism transmitter cancer cells impart receiver cancer cells with resistance to secondary metabolic, pharmacologic and genotoxic stress, providing survival advantage. The implications of this finding are briefly discussed.
Language	English
Publishing date	2018-04-19
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2017.1356898
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A community affair in the tumor microenvironment.

Rodvold, Jeffrey J / Kesari, Santosh / Zanetti, Maurizio

Oncotarget

2017 Volume 8, Issue 63, Page(s) 106173–106174

Language	English
Publishing date	2017-11-21
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.22586
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Article ; Online: Tumor microenvironment on the move and the Aselli connection.

Rodvold, Jeffrey J / Zanetti, Maurizio

Science signaling

2016 Volume 9, Issue 434, Page(s) fs13

Abstract: The tumor microenvironment is involved in many activities that promote tumor cell growth, local spreading, and metastasis. In this issue of Science Signaling, Jung et al found that lymphangiogenesis may result from the cooperation of two molecules, ... ...

Abstract	The tumor microenvironment is involved in many activities that promote tumor cell growth, local spreading, and metastasis. In this issue of Science Signaling, Jung et al found that lymphangiogenesis may result from the cooperation of two molecules, sphingosine-1-phosphate (S1P) and lipocalin 2 (LCN2), produced by tumor cells and macrophages, respectively. The new S1P-LCN2 axis stresses the importance of innate immunity in remodeling the tumor microenvironment and in lymphangiogenesis.
Language	English
Publishing date	2016-06-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.aag2279
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Article ; Online: Immune modulation by ER stress and inflammation in the tumor microenvironment.

Rodvold, Jeffrey J / Mahadevan, Navin R / Zanetti, Maurizio

Cancer letters

2016 Volume 380, Issue 1, Page(s) 227–236

Abstract: It is now increasingly evident that the immune system represents a barrier to tumor emergence, growth, and recurrence. Although this idea was originally proposed almost 50 years ago as the "immune surveillance hypothesis", it is commonly recognized that, ...

Abstract	It is now increasingly evident that the immune system represents a barrier to tumor emergence, growth, and recurrence. Although this idea was originally proposed almost 50 years ago as the "immune surveillance hypothesis", it is commonly recognized that, with few rare exceptions, tumor cells always prevail. Thus, one of the central unsolved paradoxes of tumor immunology is how a tumor escapes immune control, which is reflected in the lack of effective autochthonous or vaccine-induced anti-tumor T cell responses. In this review, we discuss the role of the endoplasmic reticulum (ER) stress response/unfolded protein response (UPR) in the immunomodulation of myeloid cells and T cells. Specifically, we will discuss how the tumor cell UPR polarizes myeloid cells in a cell-extrinsic manner, and how in turn, thus polarized myeloid cells negatively affect T cell activation and clonal expansion.
MeSH term(s)	Adaptive Immunity ; Animals ; Antigen Presentation ; Cytokines/immunology ; Cytokines/metabolism ; Endoplasmic Reticulum/immunology ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum/pathology ; Endoplasmic Reticulum Stress ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/pathology ; Inflammation Mediators/immunology ; Inflammation Mediators/metabolism ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Signal Transduction ; Tumor Escape ; Tumor Microenvironment ; Unfolded Protein Response
Chemical Substances	Cytokines ; Inflammation Mediators
Language	English
Publishing date	2016--28
Publishing country	Ireland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2015.09.009
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Article ; Online: Photopiperazines A-D, Photosensitive Interconverting Diketopiperazines with Significant and Selective Activity against U87 Glioblastoma Cells, from a Rare, Marine-Derived Actinomycete of the Family Streptomycetaceae.

Kim, Min Cheol / Cullum, Reiko / Machado, Henrique / Smith, Alexander J / Yang, Inho / Rodvold, Jeffrey J / Fenical, William

Journal of natural products

2019 Volume 82, Issue 8, Page(s) 2262–2267

Abstract: Photopiperazines A-D ( ...

Abstract	Photopiperazines A-D (
MeSH term(s)	Actinobacteria/metabolism ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Cell Line, Tumor ; Drug Screening Assays, Antitumor ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Humans ; Piperazines/chemistry ; Streptomycetaceae/chemistry
Chemical Substances	Piperazines
Language	English
Publishing date	2019-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	304325-3
ISSN	1520-6025 ; 0163-3864
ISSN (online)	1520-6025
ISSN	0163-3864
DOI	10.1021/acs.jnatprod.9b00429
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Zs.A 1144: Show issues

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Article ; Online: Extracellular vesicles produced in B cells deliver tumor suppressor miR-335 to breast cancer cells disrupting oncogenic programming in vitro and in vivo.

Almanza, Gonzalo / Rodvold, Jeffrey J / Tsui, Brian / Jepsen, Kristen / Carter, Hannah / Zanetti, Maurizio

Scientific reports

2018 Volume 8, Issue 1, Page(s) 17581

Abstract: The successful implementation of miRNA (miR) therapies in humans will ultimately rely on the use of vehicles with improved cellular delivery capability. Here we tested a new system that leverages extracellular vesicles (EVs) laden with a tumor suppressor ...

Abstract	The successful implementation of miRNA (miR) therapies in humans will ultimately rely on the use of vehicles with improved cellular delivery capability. Here we tested a new system that leverages extracellular vesicles (EVs) laden with a tumor suppressor miRNA (miR-335) produced in B cells by plasmid DNA induction (iEVs). We demonstrate that iEVs-335 efficiently and durably restored the endogenous miR-335 pool in human triple negative breast cancer cells, downregulated the expression of the miR-335 target gene SOX4 transcription factor, and markedly inhibited tumor growth in vivo. Remarkably, iEVs-335 mediated transcriptional effects that persisted in tumors after 60 days post orthotopic implantation. Genome-wide RNASeq analysis of cancer cells treated in vitro with iEVs-335 showed the regulation of a discrete number of genes only, without broad transcriptome perturbations. This new technology may be ideally suited for therapies aimed to restore tumor suppressor miRNAs in cancer cells, disrupting the oncogenic program established after escape from miRNA control.
MeSH term(s)	Animals ; B-Lymphocytes/metabolism ; Carcinogenesis/drug effects ; Cell Line, Tumor ; Extracellular Vesicles/metabolism ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Mice ; Mice, Inbred NOD ; MicroRNAs/genetics ; SOXC Transcription Factors/metabolism ; Signal Transduction/drug effects ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/therapy ; Xenograft Model Antitumor Assays
Chemical Substances	MIRN335 microRNA, human ; MicroRNAs ; SOX4 protein, human ; SOXC Transcription Factors
Language	English
Publishing date	2018-12-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-35968-2
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Article: A Janus-faced role of the unfolded protein response in antitumor immunity.

Mahadevan, Navin R / Rodvold, Jeffrey J / Zanetti, Maurizio

Oncoimmunology

2013 Volume 2, Issue 5, Page(s) e23901

Abstract: The unfolded protein response (UPR) has been established as a cell-intrinsic mechanism of survival for malignant cells facing microenvironmental stressors. Recent evidence indicates that the UPR also modulates antitumor immunity. Here, we discuss the bi- ... ...

Abstract	The unfolded protein response (UPR) has been established as a cell-intrinsic mechanism of survival for malignant cells facing microenvironmental stressors. Recent evidence indicates that the UPR also modulates antitumor immunity. Here, we discuss the bi-faced role of the UPR as it both promotes and antagonizes antitumor T-cell immunity.
Language	English
Publishing date	2013-04-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2645309-5
ISSN	2162-402X ; 2162-4011
ISSN (online)	2162-402X
ISSN	2162-4011
DOI	10.4161/onci.23901
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Article ; Online: Extracellular vesicles produced in B cells deliver tumor suppressor miR-335 to breast cancer cells disrupting oncogenic programming in vitro and in vivo

Gonzalo Almanza / Jeffrey J. Rodvold / Brian Tsui / Kristen Jepsen / Hannah Carter / Maurizio Zanetti

Scientific Reports, Vol 8, Iss 1, Pp 1-

2018 Volume 10

Abstract: Abstract The successful implementation of miRNA (miR) therapies in humans will ultimately rely on the use of vehicles with improved cellular delivery capability. Here we tested a new system that leverages extracellular vesicles (EVs) laden with a tumor ... ...

Abstract	Abstract The successful implementation of miRNA (miR) therapies in humans will ultimately rely on the use of vehicles with improved cellular delivery capability. Here we tested a new system that leverages extracellular vesicles (EVs) laden with a tumor suppressor miRNA (miR-335) produced in B cells by plasmid DNA induction (iEVs). We demonstrate that iEVs-335 efficiently and durably restored the endogenous miR-335 pool in human triple negative breast cancer cells, downregulated the expression of the miR-335 target gene SOX4 transcription factor, and markedly inhibited tumor growth in vivo. Remarkably, iEVs-335 mediated transcriptional effects that persisted in tumors after 60 days post orthotopic implantation. Genome-wide RNASeq analysis of cancer cells treated in vitro with iEVs-335 showed the regulation of a discrete number of genes only, without broad transcriptome perturbations. This new technology may be ideally suited for therapies aimed to restore tumor suppressor miRNAs in cancer cells, disrupting the oncogenic program established after escape from miRNA control.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2018-12-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: IRE1α and IGF signaling predict resistance to an endoplasmic reticulum stress-inducing drug in glioblastoma cells.

Rodvold, Jeffrey J / Xian, Su / Nussbacher, Julia / Tsui, Brian / Cameron Waller, T / Searles, Stephen C / Lew, Alyssa / Jiang, Pengfei / Babic, Ivan / Nomura, Natsuko / Lin, Jonathan H / Kesari, Santosh / Carter, Hannah / Zanetti, Maurizio

Scientific reports

2020 Volume 10, Issue 1, Page(s) 8348

Abstract: To date current therapies of glioblastoma multiforme (GBM) are largely ineffective. The induction of apoptosis by an unresolvable unfolded protein response (UPR) represents a potential new therapeutic strategy. Here we tested 12ADT, a sarcoendoplasmic ... ...

Abstract	To date current therapies of glioblastoma multiforme (GBM) are largely ineffective. The induction of apoptosis by an unresolvable unfolded protein response (UPR) represents a potential new therapeutic strategy. Here we tested 12ADT, a sarcoendoplasmic reticulum Ca
MeSH term(s)	Adult ; Apoptosis/drug effects ; Brain/pathology ; Brain/surgery ; Brain Neoplasms/drug therapy ; Brain Neoplasms/genetics ; Brain Neoplasms/mortality ; Brain Neoplasms/surgery ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; Endoplasmic Reticulum Stress/drug effects ; Endoribonucleases/genetics ; Endoribonucleases/metabolism ; Gene Expression Regulation, Neoplastic ; Glioblastoma/drug therapy ; Glioblastoma/genetics ; Glioblastoma/mortality ; Glioblastoma/surgery ; Humans ; Insulin-Like Growth Factor Binding Protein 3/genetics ; Insulin-Like Growth Factor Binding Protein 3/metabolism ; Insulin-Like Growth Factor Binding Protein 5/genetics ; Insulin-Like Growth Factor Binding Protein 5/metabolism ; Primary Cell Culture ; Progression-Free Survival ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; RNA-Seq ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/antagonists & inhibitors ; Signal Transduction/genetics ; Spheroids, Cellular ; Thapsigargin/analogs & derivatives ; Thapsigargin/pharmacology ; Thapsigargin/therapeutic use ; Tumor Cells, Cultured ; Unfolded Protein Response/drug effects
Chemical Substances	IGFBP3 protein, human ; IGFBP5 protein, human ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor Binding Protein 5 ; Thapsigargin (67526-95-8) ; ERN1 protein, human (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Endoribonucleases (EC 3.1.-) ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8)
Language	English
Publishing date	2020-05-20
Publishing country	England
Document type	Journal Article ; Observational Study ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-65320-6
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Article ; Online: IRE1α regulates macrophage polarization, PD-L1 expression, and tumor survival.

Batista, Alyssa / Rodvold, Jeffrey J / Xian, Su / Searles, Stephen C / Lew, Alyssa / Iwawaki, Takao / Almanza, Gonzalo / Waller, T Cameron / Lin, Jonathan / Jepsen, Kristen / Carter, Hannah / Zanetti, Maurizio

PLoS biology

2020 Volume 18, Issue 6, Page(s) e3000687

Abstract: In the tumor microenvironment, local immune dysregulation is driven in part by macrophages and dendritic cells that are polarized to a mixed proinflammatory/immune-suppressive phenotype. The unfolded protein response (UPR) is emerging as the possible ... ...

Abstract	In the tumor microenvironment, local immune dysregulation is driven in part by macrophages and dendritic cells that are polarized to a mixed proinflammatory/immune-suppressive phenotype. The unfolded protein response (UPR) is emerging as the possible origin of these events. Here we report that the inositol-requiring enzyme 1 (IRE1α) branch of the UPR is directly involved in the polarization of macrophages in vitro and in vivo, including the up-regulation of interleukin 6 (IL-6), IL-23, Arginase1, as well as surface expression of CD86 and programmed death ligand 1 (PD-L1). Macrophages in which the IRE1α/X-box binding protein 1 (Xbp1) axis is blocked pharmacologically or deleted genetically have significantly reduced polarization and CD86 and PD-L1 expression, which was induced independent of IFNγ signaling, suggesting a novel mechanism in PD-L1 regulation in macrophages. Mice with IRE1α- but not Xbp1-deficient macrophages showed greater survival than controls when implanted with B16.F10 melanoma cells. Remarkably, we found a significant association between the IRE1α gene signature and CD274 gene expression in tumor-infiltrating macrophages in humans. RNA sequencing (RNASeq) analysis showed that bone marrow-derived macrophages with IRE1α deletion lose the integrity of the gene connectivity characteristic of regulated IRE1α-dependent decay (RIDD) and the ability to activate CD274 gene expression. Thus, the IRE1α/Xbp1 axis drives the polarization of macrophages in the tumor microenvironment initiating a complex immune dysregulation leading to failure of local immune surveillance.
MeSH term(s)	Animals ; B7-H1 Antigen/metabolism ; CD11b Antigen/metabolism ; Cell Line, Tumor ; Cell Polarity ; Cell Proliferation ; Cell Survival ; Endoribonucleases/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Inflammation/pathology ; Linear Models ; Macrophages/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Cells/metabolism ; Neoplasms/metabolism ; Neoplasms/pathology ; Phenotype ; Protein Serine-Threonine Kinases/metabolism ; Unfolded Protein Response ; X-Box Binding Protein 1/metabolism
Chemical Substances	B7-H1 Antigen ; CD11b Antigen ; CD274 protein, human ; Cd274 protein, mouse ; X-Box Binding Protein 1 ; Xbp1 protein, mouse ; ERN1 protein, human (EC 2.7.11.1) ; Ern1 protein, mouse (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Endoribonucleases (EC 3.1.-)
Language	English
Publishing date	2020-06-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3000687
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