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Article: Regeneration of injured tissue: stem cell dynamics at interplay with mTORC1.

Mikula, Mario

2018 Volume 5, Page(s) 27

Language	English
Publishing date	2018-08-30
Publishing country	China
Document type	Editorial ; Comment
ZDB-ID	2884645-X
ISSN	2313-0792 ; 2306-9759
ISSN (online)	2313-0792
ISSN	2306-9759
DOI	10.21037/sci.2018.08.01
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Dynamic regulation of tumour progression by phenotype-switching drivers.

Vock, Laurenz / Gschwendtner, Anna / Eckel, Oliver / Mirea, Madalina A / Hengstschläger, Markus / Mikula, Mario

Clinical and translational medicine

2022 Volume 12, Issue 7, Page(s) e840

MeSH term(s)	Epithelial-Mesenchymal Transition ; Humans ; Neoplastic Processes ; Phenotype
Language	English
Publishing date	2022-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2697013-2
ISSN	2001-1326 ; 2001-1326
ISSN (online)	2001-1326
ISSN	2001-1326
DOI	10.1002/ctm2.840
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Article: Insights into Differentiation of Melanocytes from Human Stem Cells and Their Relevance for Melanoma Treatment.

Mirea, Madalina A / Eckensperger, Stefan / Hengstschläger, Markus / Mikula, Mario

Cancers

2020 Volume 12, Issue 9

Abstract: Malignant melanoma represents a highly aggressive form of skin cancer. The metastatic process itself is mostly governed by the so-called epithelial mesenchymal transition (EMT), which confers cancer cells migrative, invasive and resistance abilities. ... ...

Abstract	Malignant melanoma represents a highly aggressive form of skin cancer. The metastatic process itself is mostly governed by the so-called epithelial mesenchymal transition (EMT), which confers cancer cells migrative, invasive and resistance abilities. Since EMT represents a conserved developmental process, it is worthwhile further examining the nature of early developmental steps fundamental for melanocyte differentiation. This can be done either
Language	English
Publishing date	2020-09-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12092508
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Article: Plasma Membrane Lipids: An Important Binding Site for All Lipoprotein Classes.

Axmann, Markus / Plochberger, Birgit / Mikula, Mario / Weber, Florian / Strobl, Witta Monika / Stangl, Herbert

Membranes

2021 Volume 11, Issue 11

Abstract: Cholesterol is one of the main constituents of plasma membranes; thus, its supply is of utmost importance. This review covers the known mechanisms of cholesterol transfer from circulating lipoprotein particles to the plasma membrane, and vice versa. To ... ...

Abstract	Cholesterol is one of the main constituents of plasma membranes; thus, its supply is of utmost importance. This review covers the known mechanisms of cholesterol transfer from circulating lipoprotein particles to the plasma membrane, and vice versa. To achieve homeostasis, the human body utilizes cellular de novo synthesis and extracellular transport particles for supply of cholesterol and other lipids via the blood stream. These lipoprotein particles can be classified according to their density: chylomicrons, very low, low, and high-density lipoprotein (VLDL, LDL, and HDL, respectively). They deliver and receive their lipid loads, most importantly cholesterol, to and from cells by several redundant routes. Defects in one of these pathways (e.g., due to mutations in receptors) usually are not immediately fatal. Several redundant pathways, at least temporarily, compensate for the loss of one or more of them, but the defects trigger systemic diseases, such as atherosclerosis later on. Recently, intracellular membrane-membrane contact sites were shown to be involved in intracellular cholesterol transfer and the plasma membrane itself has been proposed to act as a binding site for lipoprotein-mediated cargo unloading.
Language	English
Publishing date	2021-11-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ISSN	2077-0375
ISSN	2077-0375
DOI	10.3390/membranes11110882
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Article ; Online: Proteome analysis of NRF2 inhibition in melanoma reveals CD44 up-regulation and increased apoptosis resistance upon vemurafenib treatment.

Weitzenböck, Hans Peter / Gschwendtner, Anna / Wiesner, Christoph / Depke, Maren / Schmidt, Frank / Trautinger, Franz / Hengstschläger, Markus / Hundsberger, Harald / Mikula, Mario

Cancer medicine

2021 Volume 11, Issue 4, Page(s) 956–967

Abstract: Malignant melanoma is the deadliest form of skin cancer and NRF2 has been proposed as a main regulator of tumor cell malignancy. Still the mechanisms how NRF2 is contributing to melanoma progression are incompletely understood. Here we analyzed the ... ...

Abstract	Malignant melanoma is the deadliest form of skin cancer and NRF2 has been proposed as a main regulator of tumor cell malignancy. Still the mechanisms how NRF2 is contributing to melanoma progression are incompletely understood. Here we analyzed the effects of either NRF2 induction or depletion, and we also quantified changes on the whole cell proteome level. Our results showed that inhibition of NRF2 leads to a loss of reactive oxygen species protection, but at the same time to an induction of an epithelial mesenchymal transition (EMT) phenotype and an up-regulation of the stem cell marker CD44. Additionally, cells devoid of NRF2 showed increased cell viability after treatment with a MYC and a BRAF inhibitor. Importantly, survival upon vemurafenib treatment was dependent on CD44 expression. Finally, analysis of archival melanoma patient samples confirmed a vice versa relationship of NRF2 and CD44 expression. In summary, we recorded changes in the proteome after NRF2 modulation in melanoma cells. Surprisingly, we identified that NRF2 inhibition lead to induction of an EMT phenotype and an increase in survival of cells after apoptosis induction. Therefore, we propose that it is important for future therapies targeting NRF2 to consider blocking EMT promoting pathways in order to achieve efficient tumor therapy.
MeSH term(s)	Apoptosis ; Cell Line, Tumor ; Humans ; Hyaluronan Receptors/genetics ; Hyaluronan Receptors/metabolism ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/metabolism ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Proteome/metabolism ; Proto-Oncogene Proteins B-raf/genetics ; Up-Regulation ; Vemurafenib/pharmacology
Chemical Substances	CD44 protein, human ; Hyaluronan Receptors ; NF-E2-Related Factor 2 ; Proteome ; Vemurafenib (207SMY3FQT) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2021-12-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2659751-2
ISSN	2045-7634 ; 2045-7634
ISSN (online)	2045-7634
ISSN	2045-7634
DOI	10.1002/cam4.4506
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Article ; Online: Rapamycin Maintains the Chondrocytic Phenotype and Interferes with Inflammatory Cytokine Induced Processes.

De Luna-Preitschopf, Andrea / Zwickl, Hannes / Nehrer, Stefan / Hengstschläger, Markus / Mikula, Mario

International journal of molecular sciences

2017 Volume 18, Issue 7

Abstract: Osteoarthritis (OA) is hallmarked by a progressive degradation of articular cartilage. Besides risk factors including trauma, obesity or genetic predisposition, inflammation has a major impact on the development of this chronic disease. During the course ...

Abstract	Osteoarthritis (OA) is hallmarked by a progressive degradation of articular cartilage. Besides risk factors including trauma, obesity or genetic predisposition, inflammation has a major impact on the development of this chronic disease. During the course of inflammation, cytokines such as tumor necrosis factor-alpha(TNF-α) and interleukin (IL)-1β are secreted by activated chondrocytes as well as synovial cells and stimulate the production of other inflammatory cytokines and matrix degrading enzymes. The mTORC1 inhibitor rapamycin is a clinical approved immunosuppressant and several studies also verified its chondroprotective effects in OA. However, the effect of blocking the mechanistic target of rapamycin complex (mTORC)1 on the inflammatory status within OA is not well studied. Therefore, we aimed to investigate if inhibition of mTORC1 by rapamycin can preserve and sustain chondrocytes in an inflammatory environment. Patient-derived chondrocytes were cultured in media supplemented with or without the mTORC1 inhibitor rapamycin. To establish an inflammatory environment, either TNF-α or IL-1β was added to the media (=OA-model). The chondroprotective and anti-inflammatory effects of rapamycin were evaluated using sulfated glycosaminoglycan (sGAG) release assay, Caspase 3/7 activity assay, lactate dehydrogenase (LDH) assay and quantitative real time polymerase chain reaction (PCR). Blocking mTORC1 by rapamycin reduced the release and therefore degradation of sGAGs, which are components of the extracellular matrix secreted by chondrocytes. Furthermore, blocking mTORC1 in OA chondrocytes resulted in an enhanced expression of the main chondrogenic markers. Rapamycin was able to protect chondrocytes from cell death in an OA-model shown by reduced Caspase 3/7 activity and diminished LDH release. Furthermore, inhibition of mTORC1 preserved the chondrogenic phenotype of OA chondrocytes, but also reduced inflammatory processes within the OA-model. This study highlights that blocking mTORC1 is a new and promising approach for treating OA. Low side effects make rapamycin an attractive implementation to existing therapeutic strategies. We showed that rapamycin's chondroprotective property might be due to an interference with IL-1β triggered inflammatory processes.
MeSH term(s)	Caspase 3/metabolism ; Caspase 7/metabolism ; Cells, Cultured ; Chondrocytes/drug effects ; Collagen Type I/metabolism ; Cytokines/pharmacology ; Glycosaminoglycans/metabolism ; Humans ; Hydrogel, Polyethylene Glycol Dimethacrylate/chemistry ; Immunohistochemistry ; L-Lactate Dehydrogenase/metabolism ; Osteoarthritis/metabolism ; Sirolimus/pharmacology ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Collagen Type I ; Cytokines ; Glycosaminoglycans ; Tumor Necrosis Factor-alpha ; Hydrogel, Polyethylene Glycol Dimethacrylate (25852-47-5) ; A73025 (268AW7000T) ; L-Lactate Dehydrogenase (EC 1.1.1.27) ; Caspase 3 (EC 3.4.22.-) ; Caspase 7 (EC 3.4.22.-) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2017-07-11
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/ijms18071494
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Article ; Online: Effects of the mTOR inhibitor everolimus and the PI3K/mTOR inhibitor NVP-BEZ235 in murine acute lung injury models.

Üstün, Sevdican / Lassnig, Caroline / Preitschopf, Andrea / Mikula, Mario / Müller, Mathias / Hengstschläger, Markus / Weichhart, Thomas

Transplant immunology

2015 Volume 33, Issue 1, Page(s) 45–50

Abstract: The mammalian target of rapamycin (mTOR) is a key signaling kinase associated with a variety of cellular functions including the regulation of immunological and inflammatory responses. Classic mTOR inhibitors such as rapamycin or everolimus are commonly ... ...

Abstract	The mammalian target of rapamycin (mTOR) is a key signaling kinase associated with a variety of cellular functions including the regulation of immunological and inflammatory responses. Classic mTOR inhibitors such as rapamycin or everolimus are commonly used in transplant as well as cancer patients to prevent transplant rejection or cancer progression, respectively. Noninfectious drug-induced pneumonitis is a frequent side effect in mTOR-inhibitor-treated patients. Therefore, we tested the effects of the mTOR inhibitor everolimus and the novel dual PI3K/mTOR inhibitor NVP-BEZ235 in a murine lipopolysaccharide (LPS)-induced acute lung injury model. C57BL/6 mice were treated with either everolimus or NVP-BEZ235 on two consecutive days prior to intratracheal administration of LPS. LPS administration induced a significant increase in total cell, neutrophil and erythrocyte numbers in the bronchoalveolar lavage fluid. Histological examination revealed a serious lung injury as shown by interstitial edema, vascular congestion and mononuclear cell infiltration in these mice after 24h. Everolimus as well as NVP-BEZ235 did not noticeably affect overall histopathology of the lungs in the lung injury model. However, NVP-BEZ235 enhanced IL-6 and TNF-α expression after 24h. In contrast, everolimus did not affect IL-6 and TNF-α levels. Interestingly, both inhibitors reduced inflammatory cytokines in an LPS/oleic acid-induced lung injury model. In conclusion, the mTOR inhibitors did not worsen the overall histopathological severity, but they exerted distinct effects on proinflammatory cytokine expression in the lung depending on the lung injury model applied.
MeSH term(s)	Acute Lung Injury/chemically induced ; Acute Lung Injury/drug therapy ; Acute Lung Injury/immunology ; Animals ; Disease Models, Animal ; Everolimus/pharmacology ; Female ; Humans ; Imidazoles/pharmacology ; Interleukin-6/immunology ; Lipopolysaccharides/toxicity ; Mice ; Oleic Acid/toxicity ; Phosphatidylinositol 3-Kinases/immunology ; Phosphoinositide-3 Kinase Inhibitors ; Quinolines/pharmacology ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; TOR Serine-Threonine Kinases/immunology ; Tumor Necrosis Factor-alpha/immunology
Chemical Substances	Imidazoles ; Interleukin-6 ; Lipopolysaccharides ; Phosphoinositide-3 Kinase Inhibitors ; Quinolines ; Tumor Necrosis Factor-alpha ; Oleic Acid (2UMI9U37CP) ; Everolimus (9HW64Q8G6G) ; mTOR protein, mouse (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; dactolisib (RUJ6Z9Y0DT)
Language	English
Publishing date	2015-06-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1160846-8
ISSN	1878-5492 ; 0966-3274
ISSN (online)	1878-5492
ISSN	0966-3274
DOI	10.1016/j.trim.2015.06.001
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Article ; Online: The unfolded protein response impacts melanoma progression by enhancing FGF expression and can be antagonized by a chemical chaperone.

Eigner, Karin / Filik, Yüksel / Mark, Florian / Schütz, Birgit / Klambauer, Günter / Moriggl, Richard / Hengstschläger, Markus / Stangl, Herbert / Mikula, Mario / Röhrl, Clemens

Scientific reports

2017 Volume 7, Issue 1, Page(s) 17498

Abstract: The mechanisms hallmarking melanoma progression are insufficiently understood. Here we studied the impact of the unfolded protein response (UPR) - a signalling cascade playing ambiguous roles in carcinogenesis - in melanoma malignancy. We identified ... ...

Abstract	The mechanisms hallmarking melanoma progression are insufficiently understood. Here we studied the impact of the unfolded protein response (UPR) - a signalling cascade playing ambiguous roles in carcinogenesis - in melanoma malignancy. We identified isogenic patient-derived melanoma cell lines harboring BRAF
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Biomarkers, Tumor/metabolism ; Butylamines/pharmacology ; Cell Line, Tumor ; Cell Movement/physiology ; Cell Survival/drug effects ; Cell Survival/physiology ; Disease Progression ; Endoplasmic Reticulum Stress/physiology ; Fibroblast Growth Factors/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/physiology ; Humans ; Melanocytes/drug effects ; Melanocytes/metabolism ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/metabolism ; Mice ; Mutation ; Neoplasm Transplantation ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins B-raf/metabolism ; Unfolded Protein Response/drug effects
Chemical Substances	4-phenylbutylamine ; Antineoplastic Agents ; Biomarkers, Tumor ; Butylamines ; Fibroblast Growth Factors (62031-54-3) ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2017-12-13
Publishing country	England
Document type	Journal Article ; 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/s41598-017-17888-9
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Article ; Online: Loss of SR-BI Down-Regulates MITF and Suppresses Extracellular Vesicle Release in Human Melanoma.

Kinslechner, Katharina / Schütz, Birgit / Pistek, Martina / Rapolter, Philipp / Weitzenböck, Hans P / Hundsberger, Harald / Mikulits, Wolfgang / Grillari, Johannes / Röhrl, Clemens / Hengstschläger, Markus / Stangl, Herbert / Mikula, Mario

International journal of molecular sciences

2019 Volume 20, Issue 5

Abstract: Melanoma is a skin tumor with a high tendency for metastasis and thus is one of the deadliest cancers worldwide. Here, we investigated the expression of the scavenger receptor class B type 1 (SR-BI), a high-density lipoprotein (HDL) receptor, and tested ... ...

Abstract	Melanoma is a skin tumor with a high tendency for metastasis and thus is one of the deadliest cancers worldwide. Here, we investigated the expression of the scavenger receptor class B type 1 (SR-BI), a high-density lipoprotein (HDL) receptor, and tested for its role in melanoma pigmentation as well as extracellular vesicle release. We first analyzed the expression of
MeSH term(s)	Cell Line, Tumor ; Down-Regulation ; Extracellular Vesicles/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Melanoma/genetics ; Melanoma/metabolism ; Microphthalmia-Associated Transcription Factor/genetics ; Microphthalmia-Associated Transcription Factor/metabolism ; Proto-Oncogene Mas ; Scavenger Receptors, Class B/genetics ; Scavenger Receptors, Class B/metabolism ; Synaptosomal-Associated Protein 25/genetics ; Synaptosomal-Associated Protein 25/metabolism ; Vesicular Transport Proteins/genetics ; Vesicular Transport Proteins/metabolism ; rab GTP-Binding Proteins/genetics ; rab GTP-Binding Proteins/metabolism
Chemical Substances	MAS1 protein, human ; MITF protein, human ; Microphthalmia-Associated Transcription Factor ; Proto-Oncogene Mas ; SCARB1 protein, human ; SNAP25 protein, human ; Scavenger Receptors, Class B ; Synaptosomal-Associated Protein 25 ; Vesicular Transport Proteins ; Vps25 protein, human ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2019-03-01
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/ijms20051063
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Article ; Online: Generation of metastatic melanoma specific antibodies by affinity purification.

Schütz, Birgit / Koppensteiner, Anita / Schörghofer, David / Kinslechner, Katharina / Timelthaler, Gerald / Eferl, Robert / Hengstschläger, Markus / Missbichler, Albert / Hundsberger, Harald / Mikula, Mario

Scientific reports

2016 Volume 6, Page(s) 37253

Abstract: Melanoma is the most aggressive type of skin cancer and one of the most frequent tumours in young adults. Identification of primary tumours prone to develop metastasis is of paramount importance for further patient stratification. However, till today, no ...

Abstract	Melanoma is the most aggressive type of skin cancer and one of the most frequent tumours in young adults. Identification of primary tumours prone to develop metastasis is of paramount importance for further patient stratification. However, till today, no markers exist that are routinely used to predict melanoma progression. To ameliorate this problem, we generated antiserum directed against metastatic melanoma tissue lysate and applied a novel approach to purify the obtained serum via consecutive affinity chromatography steps. The established antibody, termed MHA-3, showed high reactivity against metastatic melanoma cell lines both in vitro and in vivo. We also tested MHA-3 on 227 melanoma patient samples and compared staining with the melanoma marker S100b. Importantly, MHA-3 was able to differentiate between metastatic and non-metastatic melanoma samples. By proteome analysis we identified 18 distinct antigens bound by MHA-3. Combined expression profiling of all identified proteins revealed a significant survival difference in melanoma patients. In conclusion, we developed a polyclonal antibody, which is able to detect metastatic melanoma on paraffin embedded sections. Hence, we propose that this antibody will represent a valuable additional tool for precise melanoma diagnosis.
MeSH term(s)	Animals ; Antibodies, Neoplasm/chemistry ; Antibodies, Neoplasm/immunology ; Antibodies, Neoplasm/isolation & purification ; Antigens, Neoplasm/chemistry ; Antigens, Neoplasm/immunology ; Biomarkers, Tumor/chemistry ; Biomarkers, Tumor/immunology ; Chromatography, Affinity ; Female ; Humans ; Melanoma/immunology ; Melanoma/mortality ; Melanoma/pathology ; Mice ; Mice, SCID ; Neoplasm Metastasis ; Rabbits
Chemical Substances	Antibodies, Neoplasm ; Antigens, Neoplasm ; Biomarkers, Tumor
Language	English
Publishing date	2016-11-17
Publishing country	England
Document type	Journal Article ; 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/srep37253
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