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Article ; Online: Dialog beyond the Grave: Necrosis in the Tumor Microenvironment and Its Contribution to Tumor Growth.

Zapletal, Emilija / Vasiljevic, Tea / Busson, Pierre / Matijevic Glavan, Tanja

International journal of molecular sciences

2023 Volume 24, Issue 6

Abstract: Damage-associated molecular patterns (DAMPs) are endogenous molecules released from the necrotic cells dying after exposure to various stressors. After binding to their receptors, they can stimulate various signaling pathways in target cells. DAMPs are ... ...

Abstract	Damage-associated molecular patterns (DAMPs) are endogenous molecules released from the necrotic cells dying after exposure to various stressors. After binding to their receptors, they can stimulate various signaling pathways in target cells. DAMPs are especially abundant in the microenvironment of malignant tumors and are suspected to influence the behavior of malignant and stromal cells in multiple ways often resulting in promotion of cell proliferation, migration, invasion, and metastasis, as well as increased immune evasion. This review will start with a reminder of the main features of cell necrosis, which will be compared to other forms of cell death. Then we will summarize the various methods used to assess tumor necrosis in clinical practice including medical imaging, histopathological examination, and/or biological assays. We will also consider the importance of necrosis as a prognostic factor. Then the focus will be on the DAMPs and their role in the tumor microenvironment (TME). We will address not only their interactions with the malignant cells, frequently leading to cancer progression, but also with the immune cells and their contribution to immunosuppression. Finally, we will emphasize the role of DAMPs released by necrotic cells in the activation of Toll-like receptors (TLRs) and the possible contributions of TLRs to tumor development. This last point is very important for the future of cancer therapeutics since there are attempts to use TLR artificial ligands for cancer therapeutics.
MeSH term(s)	Humans ; Tumor Microenvironment ; Neoplasms/metabolism ; Necrosis ; Toll-Like Receptors/metabolism ; Signal Transduction
Chemical Substances	Toll-Like Receptors
Language	English
Publishing date	2023-03-09
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/ijms24065278
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Article ; Online: Necrotic Cells from Head and Neck Carcinomas Release Biomolecules That Are Activating Toll-like Receptor 3.

Vasiljevic, Tea / Tarle, Marko / Hat, Koraljka / Luksic, Ivica / Mikulandra, Martina / Busson, Pierre / Matijevic Glavan, Tanja

International journal of molecular sciences

2023 Volume 24, Issue 20

Abstract: Tumor necrosis is a recurrent characteristic of head and neck squamous cell carcinomas (HNSCCs). There is a need for more investigations on the influence of biomolecules released by these necrotic foci in the HNSCC tumor microenvironment. It is suspected ...

Abstract	Tumor necrosis is a recurrent characteristic of head and neck squamous cell carcinomas (HNSCCs). There is a need for more investigations on the influence of biomolecules released by these necrotic foci in the HNSCC tumor microenvironment. It is suspected that a fraction of the biomolecules released by necrotic cells are damage-associated molecular patterns (DAMPs), which are known to be natural endogenous ligands of Toll-like receptors (TLRs), including, among others, proteins and nucleic acids. However, there has been no direct demonstration that biomolecules released by HNSCC necrotic cells can activate TLRs. Our aim was to investigate whether some of these molecules could behave as agonists of the TLR3, either in vitro or in vivo. We chose a functional approach based on reporter cell exhibiting artificial TLR3 expression and downstream release of secreted alkaline phosphatase. The production of biomolecules activating TLR3 was first investigated in vitro using three HNSCC cell lines subjected to various pronecrotic stimuli (external irradiation, serum starvation, hypoxia and oxidative stress). TLR3 agonists were also investigated in necrotic tumor fluids from five oral cancer patients and three mouse tumor grafts. The release of biomolecules activating TLR3 was demonstrated for all three HNSCC cell lines. External irradiation was the most consistently efficient stimulus, and corresponding TLR3 agonists were conveyed in extracellular vesicles. TLR3-stimulating activity was detected in the fluids from all five patients and three mouse tumor grafts. In most cases, this activity was greatly reduced by RNAse pretreatment or TLR3 blocking antibodies. Our data indicate that TLR3 agonists are consistently present in necrotic fluids from HNSCC cells and mainly made of dsRNA fragments. These endogenous agonists may induce TLR3, which might lead to a protumorigenic effect. Regarding methodological aspects, our study demonstrates that direct investigations-including functional testing-can be performed on necrotic fluids from patient tumors.
MeSH term(s)	Animals ; Humans ; Mice ; Head and Neck Neoplasms ; Necrosis/metabolism ; Squamous Cell Carcinoma of Head and Neck ; Toll-Like Receptor 3/metabolism ; Toll-Like Receptor 9 ; Toll-Like Receptors ; Tumor Microenvironment
Chemical Substances	Toll-Like Receptor 3 ; Toll-Like Receptor 9 ; Toll-Like Receptors ; TLR3 protein, human
Language	English
Publishing date	2023-10-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms242015269
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Article: The Role of Acrolein and NADPH Oxidase in the Granulocyte-Mediated Growth-Inhibition of Tumor Cells.

Jaganjac, Morana / Matijevic Glavan, Tanja / Zarkovic, Neven

Cells

2019 Volume 8, Issue 4

Abstract: ...

Abstract	:
MeSH term(s)	Acrolein/metabolism ; Animals ; Cell Line, Tumor ; Cell Proliferation ; Granulocytes/metabolism ; Granulocytes/pathology ; Male ; NADPH Oxidases/metabolism ; Oxidation-Reduction ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Toll-Like Receptor 4/metabolism
Chemical Substances	Reactive Oxygen Species ; Toll-Like Receptor 4 ; Acrolein (7864XYD3JJ) ; NADPH Oxidases (EC 1.6.3.-)
Language	English
Publishing date	2019-03-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8040292
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Article: The in vitro effect of poly (I:C) on cell morphology of a metastatic pharyngeal cell line

Matijevic Glavan, Tanja / Martina Mikulandra

Biológia. 2017 Aug. 28, v. 72, no. 8

2017

Abstract: Toll-like receptor 3 (TLR3) belongs to a family of TLRs, which are activated by ligands of bacterial and viral origin. Following ligation, TLRs induce different cellular responses including immune response, apoptosis, cell proliferation, cell migration, ... ...

Abstract	Toll-like receptor 3 (TLR3) belongs to a family of TLRs, which are activated by ligands of bacterial and viral origin. Following ligation, TLRs induce different cellular responses including immune response, apoptosis, cell proliferation, cell migration, etc. TLR3 is induced by dsRNA or its analogue poly (I:C). In our previous research, we have noticed the morphological change in Detroit 562 cells after poly (I:C) stimulation resulting in mesenchymal phenotype. Here we have studied the pathways involved in the observed phenomenon by analyzing cell morphometric parameters. We have demonstrated that the observed changed morphology is not a consequence of increased apoptosis. Rho inhibitor also did not abrogate the induced morphological change, however, it induced the formation of short sheet-like sprouts and the combination of Rho inhibitor and poly (I:C) induced lamellipodia-like structures and more filopodia-like thin antennae sprouts. Finally, we have shown that Rac1 activation and epithelial to mesenchymal transition (EMT) markers (vimentin, fibronectin and Snail) are increased after poly (I:C) stimulation. Since we have previously shown increased migration of Detroit 562 cells after poly (I:C) stimulation, we conclude here that this and the morphological change are the result of EMT and Rac1 activation.
Keywords	apoptosis ; cell lines ; cell movement ; cell proliferation ; double-stranded RNA ; epithelium ; fibronectins ; immune response ; ligands ; metastasis ; morphometry ; pharynx ; phenotype ; Toll-like receptor 3 ; vimentin
Language	English
Dates of publication	2017-0828
Size	p. 954-960.
Publishing place	De Gruyter
Document type	Article
ZDB-ID	419136-5
ISSN	1336-9563 ; 0006-3088 ; 1335-6372 ; 1335-6380
ISSN (online)	1336-9563
ISSN	0006-3088 ; 1335-6372 ; 1335-6380
DOI	10.1515/biolog-2017-0103
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Article ; Online: Oxidative Stress and Cancer Heterogeneity Orchestrate NRF2 Roles Relevant for Therapy Response.

Gall Trošelj, Koraljka / Tomljanović, Marko / Jaganjac, Morana / Matijević Glavan, Tanja / Čipak Gašparović, Ana / Milković, Lidija / Borović Šunjić, Suzana / Buttari, Brigitta / Profumo, Elisabetta / Saha, Sarmistha / Saso, Luciano / Žarković, Neven

Molecules (Basel, Switzerland)

2022 Volume 27, Issue 5

Abstract: Oxidative stress and its end-products, such as 4-hydroxynonenal (HNE), initiate activation of the Nuclear Factor Erythroid 2-Related Factor 2 (NRF2)/Kelch Like ECH Associated Protein 1 (KEAP1) signaling pathway that plays a crucial role in the ... ...

Abstract	Oxidative stress and its end-products, such as 4-hydroxynonenal (HNE), initiate activation of the Nuclear Factor Erythroid 2-Related Factor 2 (NRF2)/Kelch Like ECH Associated Protein 1 (KEAP1) signaling pathway that plays a crucial role in the maintenance of cellular redox homeostasis. However, an involvement of 4-HNE and NRF2 in processes associated with the initiation of cancer, its progression, and response to therapy includes numerous, highly complex events. They occur through interactions between cancer and stromal cells. These events are dependent on many cell-type specific features. They start with the extent of NRF2 binding to its cytoplasmic repressor, KEAP1, and extend to the permissiveness of chromatin for transcription of Antioxidant Response Element (ARE)-containing genes that are NRF2 targets. This review will explore epigenetic molecular mechanisms of NRF2 transcription through the specific molecular anatomy of its promoter. It will explain the role of NRF2 in cancer stem cells, with respect to cancer therapy resistance. Additionally, it also discusses NRF2 involvement at the cross-roads of communication between tumor associated inflammatory and stromal cells, which is also an important factor involved in the response to therapy.
MeSH term(s)	Kelch-Like ECH-Associated Protein 1
Chemical Substances	Kelch-Like ECH-Associated Protein 1
Language	English
Publishing date	2022-02-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules27051468
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Article ; Online: Radio-sensitization of head and neck cancer cells by a combination of poly(I:C) and cisplatin through downregulation of survivin and c-IAP2.

Mikulandra, Martina / Kobescak, Antonio / Verillaud, Benjamin / Busson, Pierre / Matijevic Glavan, Tanja

Cellular oncology (Dordrecht)

2018 Volume 42, Issue 1, Page(s) 29–40

Abstract: Purpose: Head and neck squamous cell carcinoma (HNSCC) is one of the most common cancers. Concurrent radio-chemotherapy is the standard of care for advanced tumors. However, there is a need for more efficient regimens with less side effects resulting ... ...

Abstract	Purpose: Head and neck squamous cell carcinoma (HNSCC) is one of the most common cancers. Concurrent radio-chemotherapy is the standard of care for advanced tumors. However, there is a need for more efficient regimens with less side effects resulting from high doses. Therefore, we set out to explore the therapeutic potential of ternary combinations by bringing together irradiation, cis-platinum and a TLR3 agonist, poly(I:C), with the aim to reduce the dosage of each treatment. This approach is based on our previous work, which revealed a selective cytotoxic effect of TLR3 agonists against malignant cells when combined with other anti-neoplastic agents. Methods: We explored the survival of HNSCC-derived cells (Detroit 562, FaDu, SQ20B and Cal27) using MTT and caspase 3/7 activation assays. The radio-sensitization effects of poly(I:C) and cisplatin were assessed using Western blotting, cell cycle progression, ROS formation and qRT-PCR assays. Results: We found that the combination of poly(I:C) and cisplatin downregulated c-IAP2 and survivin expression, reduced cell survival, induced anti-apoptotic gene expression and apoptosis, increased ROS formation and induced G2/M cell cycle arrest in the HNSCC-derived cells tested. Conclusions: Our results indicate that a combined poly(I:C) and cisplatin treatment reduces the survival and induces the radio-sensitivity of HNSCC-derived cells, thus providing a rationale for the development of novel strategies for the treatment of head and neck cancer.
MeSH term(s)	Apoptosis/drug effects ; Apoptosis/genetics ; Apoptosis/radiation effects ; Cell Cycle Checkpoints/drug effects ; Cell Cycle Checkpoints/radiation effects ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/radiation effects ; Cisplatin/pharmacology ; Down-Regulation/drug effects ; Down-Regulation/radiation effects ; Gamma Rays ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/radiation effects ; Head and Neck Neoplasms/genetics ; Head and Neck Neoplasms/pathology ; Humans ; Inhibitor of Apoptosis Proteins/genetics ; Inhibitor of Apoptosis Proteins/metabolism ; Poly I-C/pharmacology ; Radiation Tolerance/drug effects ; Radiation Tolerance/radiation effects ; Reactive Oxygen Species/metabolism ; Survivin/genetics ; Survivin/metabolism
Chemical Substances	Inhibitor of Apoptosis Proteins ; Reactive Oxygen Species ; Survivin ; Poly I-C (O84C90HH2L) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2018-09-04
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2595109-9
ISSN	2211-3436 ; 1875-8606 ; 2211-3428
ISSN (online)	2211-3436
ISSN	1875-8606 ; 2211-3428
DOI	10.1007/s13402-018-0403-7
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Article: Neurotoxicity of silver nanoparticles stabilized with different coating agents: In vitro response of neuronal precursor cells

Pavičić, Ivan / Milić, Mirta / Pongrac, Igor M / Brkić Ahmed, Lada / Matijević Glavan, Tanja / Ilić, Krunoslav / Zapletal, Emilija / Ćurlin, Marija / Mitrečić, Dinko / Vinković Vrček, Ivana

Food and chemical toxicology. 2020 Feb., v. 136

2020

Abstract: Silver nanoparticles (AgNPs) represent one of the most abundant biocidal nanomaterials contained in more than 30% of nano-enabled consumer products and 75% of nanomedical products. The cumulative exposure of the general population may therefore reach ... ...

Abstract	Silver nanoparticles (AgNPs) represent one of the most abundant biocidal nanomaterials contained in more than 30% of nano-enabled consumer products and 75% of nanomedical products. The cumulative exposure of the general population may therefore reach critical and potentially hazardous levels. Due to data gaps on AgNP effects in humans, it is urgent to further evaluate their possible toxicity, particularly in vulnerable systems like the nervous one. As AgNPs may cross the blood brain and placental barriers, this study evaluated the in vitro effect of different AgNPs on neuronal precursor cells.For this purpose, 10 nm-sized AgNPs were stabilized with five different coating agents rendering a neutral, positive and negative surface charge. Murine neural stem cells (mNSCs) were used as cellular model to test AgNP neurotoxicity by evaluating the range of toxicity endpoints including cellular viability, apoptosis induction, oxidative stress response, cellular and mitochondrial membrane damages, DNA damage, inflammation response, and neural stem cell regulation.Our results clearly showed that the neurotoxic potential of AgNPs was not dependent on their surface charge or coating agents used for their surface stabilization. All AgNP types exhibited significant toxicity in neuronal precursor cells at an in vitro dose of 5 mg Ag/L or lower.
Keywords	DNA damage ; apoptosis ; blood ; brain ; cumulative exposure ; health effects assessments ; in vitro studies ; inflammation ; mice ; mitochondrial membrane ; nanosilver ; neural stem cells ; neurons ; neurotoxicity ; oxidative stress ; products and commodities ; silver ; stress response ; viability
Language	English
Dates of publication	2020-02
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2019.110935
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Article ; Online: Toll-like receptor 3 stimulation triggers metabolic reprogramming in pharyngeal cancer cell line through Myc, MAPK, and HIF.

Matijevic Glavan, Tanja / Cipak Gasparovic, Ana / Vérillaud, Benjamin / Busson, Pierre / Pavelic, Jasminka

Molecular carcinogenesis

2017 Volume 56, Issue 4, Page(s) 1214–1226

Abstract: Toll-like receptor 3 (TLR3) has a dual role in cancer; its activation can trigger apoptosis as well as stimulate cancer cell survival, proliferation, and progression. We have shown here that TLR3 activation can induce metabolic reprogramming in a ... ...

Abstract	Toll-like receptor 3 (TLR3) has a dual role in cancer; its activation can trigger apoptosis as well as stimulate cancer cell survival, proliferation, and progression. We have shown here that TLR3 activation can induce metabolic reprogramming in a pharyngeal cancer cell line, leading to increased aerobic glycolysis, cell migration, elevated levels of reactive oxidative species (ROS), and decreased anti-oxidative response. Key proteins in these signaling pathways are heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1), pyruvate kinase M2 (PKM2), and CD44 variants, which were over-expressed after TLR3 stimulation. TLR3 activation also induced upregulation of different genes involved in cancer progression (VEGF, MMP9, uPAR) and enzymes involved in glycolytic pathway. Most of the observed effects were Myc-dependent; however, some of them were also connected with MAPK and HIF signaling pathways. Since TLR3 agonists are being investigated as potential novel cancer therapy adjuvants and apoptosis inducers, alone or in combination with other therapeutic options, data presented here suggest extreme caution before their introduction into clinical practice. The fact that TLR3 ligands [poly(I:C) and poly(A:U)] can also aid cancer survival and progression, through induction of metabolic reprogramming, emphasizes the need to investigate this particular topic. Our data suggest that the combination of TLR3 ligands with Myc or MAPK inhibitors may be a way to neutralize their undesirable effects while enhancing their anti-tumor effect. © 2016 Wiley Periodicals, Inc.
MeSH term(s)	Cell Line, Tumor ; Cell Movement ; Glycolysis ; Humans ; Hypoxia-Inducible Factor 1/metabolism ; MAP Kinase Signaling System ; Oxidative Stress ; Pharyngeal Neoplasms/metabolism ; Pharyngeal Neoplasms/pathology ; Pharynx/metabolism ; Pharynx/pathology ; Poly I-C/metabolism ; Proto-Oncogene Proteins c-myc/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Toll-Like Receptor 3/metabolism
Chemical Substances	Hypoxia-Inducible Factor 1 ; Proto-Oncogene Proteins c-myc ; Reactive Oxygen Species ; TLR3 protein, human ; Toll-Like Receptor 3 ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2017-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
DOI	10.1002/mc.22584
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Article ; Online: Neurotoxicity of silver nanoparticles stabilized with different coating agents: In vitro response of neuronal precursor cells.

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

2019 Volume 136, Page(s) 110935

Abstract	Silver nanoparticles (AgNPs) represent one of the most abundant biocidal nanomaterials contained in more than 30% of nano-enabled consumer products and 75% of nanomedical products. The cumulative exposure of the general population may therefore reach critical and potentially hazardous levels. Due to data gaps on AgNP effects in humans, it is urgent to further evaluate their possible toxicity, particularly in vulnerable systems like the nervous one. As AgNPs may cross the blood brain and placental barriers, this study evaluated the in vitro effect of different AgNPs on neuronal precursor cells. For this purpose, 10 nm-sized AgNPs were stabilized with five different coating agents rendering a neutral, positive and negative surface charge. Murine neural stem cells (mNSCs) were used as cellular model to test AgNP neurotoxicity by evaluating the range of toxicity endpoints including cellular viability, apoptosis induction, oxidative stress response, cellular and mitochondrial membrane damages, DNA damage, inflammation response, and neural stem cell regulation. Our results clearly showed that the neurotoxic potential of AgNPs was not dependent on their surface charge or coating agents used for their surface stabilization. All AgNP types exhibited significant toxicity in neuronal precursor cells at an in vitro dose of 5 mg Ag/L or lower.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Cattle ; Cell Survival/drug effects ; Cetrimonium/chemistry ; Cetrimonium/toxicity ; DNA Damage/drug effects ; Dioctyl Sulfosuccinic Acid/chemistry ; Dioctyl Sulfosuccinic Acid/toxicity ; Membrane Potential, Mitochondrial/drug effects ; Metal Nanoparticles/toxicity ; Mice, Inbred C57BL ; Neural Stem Cells/drug effects ; Oxidative Stress/drug effects ; Polylysine/chemistry ; Polylysine/toxicity ; Povidone/chemistry ; Povidone/toxicity ; Serum Albumin, Bovine/chemistry ; Serum Albumin, Bovine/toxicity ; Silver/chemistry ; Silver/toxicity ; Transcriptome/drug effects
Chemical Substances	Dioctyl Sulfosuccinic Acid (10041-19-7) ; Polylysine (25104-18-1) ; Serum Albumin, Bovine (27432CM55Q) ; Silver (3M4G523W1G) ; Povidone (FZ989GH94E) ; Cetrimonium (Z7FF1XKL7A)
Language	English
Publishing date	2019-11-03
Publishing country	England
Document type	Journal Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2019.110935
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