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Article: The Role of Beclin 1-Dependent Autophagy in Cancer.

Vega-Rubín-de-Celis, Silvia

2019 Volume 9, Issue 1

Abstract: Autophagy ( ...

Abstract	Autophagy (
Language	English
Publishing date	2019-12-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology9010004
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Article: Editorial: Molecular Mechanisms of Autophagy in Cancer.

Humbert, Magali / Vega-Rubin-de-Celis, Silvia / Velasco, Guillermo / Wei, Yongjie

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 918511

Language	English
Publishing date	2022-06-17
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.918511
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Article ; Online: GRB2 is a BECN1 interacting protein that regulates autophagy.

Montero-Vergara, Jetsy / Plachetta, Kira / Kinch, Lisa / Bernhardt, Stephan / Kashyap, Kriti / Levine, Beth / Thukral, Lipi / Vetter, Martina / Thomssen, Christoph / Wiemann, Stefan / Peña-Llopis, Samuel / Jendrossek, Verena / Vega-Rubin-de-Celis, Silvia

Cell death & disease

2024 Volume 15, Issue 1, Page(s) 14

Abstract: GRB2 is an adaptor protein of HER2 (and several other tyrosine kinases), which we identified as a novel BECN1 (Beclin 1) interacting partner. GRB2 co-immunoprecipitated with BECN1 in several breast cancer cell lines and regulates autophagy through a ... ...

Abstract	GRB2 is an adaptor protein of HER2 (and several other tyrosine kinases), which we identified as a novel BECN1 (Beclin 1) interacting partner. GRB2 co-immunoprecipitated with BECN1 in several breast cancer cell lines and regulates autophagy through a mechanism involving the modulation of the class III PI3Kinase VPS34 activity. In ovo studies in a CAM (Chicken Chorioallantoic Membrane) model indicated that GRB2 knockdown, as well as overexpression of GRB2 loss-of-function mutants (Y52A and S86A-R88A) compromised tumor growth. These differences in tumor growth correlated with differential autophagy activity, indicating that autophagy effects might be related to the effects on tumorigenesis. Our data highlight a novel function of GRB2 as a BECN1 binding protein and a regulator of autophagy.
MeSH term(s)	Animals ; Adaptor Proteins, Signal Transducing ; Autophagy ; Beclin-1/metabolism ; Carcinogenesis ; Cell Transformation, Neoplastic ; Humans ; GRB2 Adaptor Protein/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Beclin-1 ; GRB2 protein, human ; BECN1 protein, human ; GRB2 Adaptor Protein
Language	English
Publishing date	2024-01-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-023-06387-7
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Article ; Online: Regulation of Beclin 1-Mediated Autophagy by Oncogenic Tyrosine Kinases.

Vega-Rubín-de-Celis, Silvia / Kinch, Lisa / Peña-Llopis, Samuel

International journal of molecular sciences

2020 Volume 21, Issue 23

Abstract: Beclin 1 is a major regulator of autophagy, and it is a core component of the class III PI3K complexes. Beclin 1 is a highly conserved protein and its function is regulated in a number of ways, including post-translational modifications. Several studies ... ...

Abstract	Beclin 1 is a major regulator of autophagy, and it is a core component of the class III PI3K complexes. Beclin 1 is a highly conserved protein and its function is regulated in a number of ways, including post-translational modifications. Several studies indicate that receptor and non-receptor tyrosine kinases regulate autophagy activity in cancer, and some suggest the importance of Beclin 1 tyrosine phosphorylation in this process. Here we summarize the current knowledge of the mechanism whereby some oncogenic tyrosine kinases regulate autophagy through Beclin 1.
MeSH term(s)	Animals ; Autophagy/genetics ; Beclin-1/chemistry ; Beclin-1/genetics ; Beclin-1/metabolism ; Gene Expression Regulation ; Humans ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Oncogene Proteins/chemistry ; Oncogene Proteins/genetics ; Oncogene Proteins/metabolism ; Phosphorylation ; Protein-Tyrosine Kinases/chemistry ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; Signal Transduction ; Structure-Activity Relationship
Chemical Substances	Beclin-1 ; Oncogene Proteins ; Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2020-12-03
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/ijms21239210
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Article ; Online: Studying Autophagy In Vivo in the Mammary Gland and in Xenograft Samples.

Zou, Zhongju / Fernández, Álvaro F / Jendrossek, Verena / Vega-Rubín-de-Celis, Silvia

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2445, Page(s) 255–272

Abstract: Autophagy is a dynamic process that can be monitored in multiple ways, both in vitro and in vivo. Studies in mice are a widely used tool to understand multiple diseases and conditions where autophagy plays a role, and therefore autophagic flux ... ...

Abstract	Autophagy is a dynamic process that can be monitored in multiple ways, both in vitro and in vivo. Studies in mice are a widely used tool to understand multiple diseases and conditions where autophagy plays a role, and therefore autophagic flux measurement in tissues of rodent models are of utmost importance. Here, we present some assays successfully used in determining the autophagy status in the mice mammary gland as well as in xenografts.
MeSH term(s)	Animals ; Autophagy ; Heterografts ; Mammary Glands, Animal ; Mice ; Microtubule-Associated Proteins ; Transplantation, Heterologous
Chemical Substances	Microtubule-Associated Proteins
Language	English
Publishing date	2021-12-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2071-7_16
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Article ; Online: TROP2 expression and SN38 antitumor activity in malignant pleural mesothelioma cells provide a rationale for antibody-drug conjugate therapy.

Hegedüs, Luca / Okumus, Özlem / Mairinger, Fabian / Ploenes, Till / Reuter, Sebastian / Schuler, Martin / Welt, Anja / Vega-Rubin-de-Celis, Silvia / Theegarten, Dirk / Bankfalvi, Agnes / Aigner, Clemens / Hegedüs, Balazs

Lung cancer (Amsterdam, Netherlands)

2023 Volume 178, Page(s) 237–246

Abstract: Objectives: Malignant pleural mesothelioma (MPM) is an aggressive cancer which at large is not amenable to curative surgery. Despite the recent approval of immune checkpoint inhibitor therapy, the response rates and survival following systemic therapy ... ...

Abstract	Objectives: Malignant pleural mesothelioma (MPM) is an aggressive cancer which at large is not amenable to curative surgery. Despite the recent approval of immune checkpoint inhibitor therapy, the response rates and survival following systemic therapy is still limited. Sacituzumab govitecan is an antibody-drug conjugate targeting the topoisomerase I inhibitor SN38 to trophoblast cell-surface antigen 2 (TROP-2)-positive cells. Here we have explored the therapeutic potential of sacituzumab govitecan in MPM models. Materials and methods: TROP2 expression was analyzed in a panel of two well established and 15 pleural effusion derived novel lines by RT-QPCR and immunoblotting, TROP2 membrane-localization was studied by flow cytometry and immunohistochemistry. Cultured mesothelial cells and pneumothorax pleura served as controls. The sensitivity of MPM cell lines to irinotecan and SN38 was studied using cell viability, cell cycle, apoptosis and DNA damage assays. Drug sensitivity of cell lines was correlated with RNA expression of DNA repair genes. Drug sensitivity was defined as an IC50 below 5 nM in the cell viability assay. Results: TROP2 expression was detected at RNA and protein level in 6 of the 17 MPM cell lines, but not in in cultured mesothelial control cells or in the mesothelial layer of the pleura. TROP2 was detectable on the cell membrane in 5 MPM lines and was present in the nucleus in 6 cell models. Ten of 17 MPM cell lines showed sensitivity to SN38 treatment, among those 4 expressed TROP2. High AURKA RNA expression and high proliferation rate correlated with sensitivity to SN38-induced cell death, DNA damage response, cell cycle arrest and cell death. Sacituzumab govitecan treatment effectively induced cell cycle arrest and cell death in TROP2-positive MPM cells. Conclusion: TROP2 expression and sensitivity to SN38 in MPM cell lines support biomarker-selected clinical exploration of sacituzumab govitecan in patients with MPM.
MeSH term(s)	Humans ; Cell Line, Tumor ; Immunoconjugates/pharmacology ; Immunoconjugates/therapeutic use ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mesothelioma/drug therapy ; Mesothelioma/genetics ; Mesothelioma/metabolism ; Mesothelioma, Malignant/drug therapy ; Pleural Neoplasms/drug therapy ; Pleural Neoplasms/genetics ; Pleural Neoplasms/metabolism ; RNA ; Irinotecan/pharmacology
Chemical Substances	Immunoconjugates ; RNA (63231-63-0) ; TACSTD2 protein, human ; Irinotecan (7673326042)
Language	English
Publishing date	2023-03-08
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	632771-0
ISSN	1872-8332 ; 0169-5002
ISSN (online)	1872-8332
ISSN	0169-5002
DOI	10.1016/j.lungcan.2023.03.003
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Zs.A 2135: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Niersch, Jennifer / Vega-Rubín-de-Celis, Silvia / Bazarna, Anna / Mergener, Svenja / Jendrossek, Verena / Siveke, Jens T / Peña-Llopis, Samuel

iScience

2021 Volume 24, Issue 3, Page(s) 102173

Abstract: Synonymous mutations are generally disregarded by genomic analyses because they are considered non-pathogenic. We identified and characterized a somatic synonymous mutation in the epigenetic modifier and tumor ... ...

Abstract	Synonymous mutations are generally disregarded by genomic analyses because they are considered non-pathogenic. We identified and characterized a somatic synonymous mutation in the epigenetic modifier and tumor suppressor
Language	English
Publishing date	2021-02-12
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2021.102173
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Article: Nintedanib and Dasatinib Treatments Induce Protective Autophagy as a Potential Resistance Mechanism in MPM Cells.

Hegedüs, Luca / Szücs, Kata D / Kudla, Matthias / Heidenreich, Julian / Jendrossek, Verena / Peña-Llopis, Samuel / Garay, Tamas / Czirok, Andras / Aigner, Clemens / Plönes, Till / Vega-Rubin-de-Celis, Silvia / Hegedüs, Balazs

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 852812

Abstract: Malignant pleural mesothelioma (MPM) is a rare type of cancer with a grim prognosis. So far, no targetable oncogenic mutation was identified in MPM and biomarkers with predictive value toward drug sensitivity or resistance are also lacking. Nintedanib ( ... ...

Abstract	Malignant pleural mesothelioma (MPM) is a rare type of cancer with a grim prognosis. So far, no targetable oncogenic mutation was identified in MPM and biomarkers with predictive value toward drug sensitivity or resistance are also lacking. Nintedanib (BIBF1120) is a small-molecule tyrosine kinase inhibitor that showed promising efficacy preclinically and in phase II trial in MPM as an angiogenesis inhibitor combined with chemotherapy. However, the extended phase III trial failed. In this study, we investigated the effect of nintedanib on one of its targets, the SRC kinase, in two commercial and six novel MPM cell lines. Surprisingly, nintedanib treatment did not inhibit SRC activation in MPM cells and even increased phosphorylation of SRC in several cell lines. Combination treatment with the SRC inhibitor dasatinib could reverse this effect in all cell lines, however, the cellular response was dependent on the drug sensitivity of the cells. In 2 cell lines, with high sensitivity to both nintedanib and dasatinib, the drug combination had no synergistic effect but cell death was initiated. In 2 cell lines insensitive to nintedanib combination treatment reduced cell viability synergisticaly without cell death. In contrast, in these cells both treatments increased the autophagic flux assessed by degradation of the autophagy substrate p62 and increased presence of LC3B-II, increased number of GFP-LC3 puncta and decreased readings of the HiBiT-LC3 reporter. Additionaly, autophagy was synergistically promoted by the combined treatment. At the transcriptional level, analysis of lysosomal biogenesis regulator Transcription Factor EB (TFEB) showed that in all cell lines treated with nintedanib and to a lesser extent, with dasatinib, it became dephosphorylated and accumulated in the nucleus. Interestingly, the expression of certain known TFEB target genes implicated in autophagy or lysosomal biogenesis were significantly modified only in 1 cell line. Finally, we showed that autophagy induction in our MPM cell lines panel by nintedanib and dasatinib is independent of the AKT/mTOR and the ERK pathways. Our study reveals that autophagy can serve as a cytoprotective mechanism following nintedanib or dasatinib treatments in MPM cells.
Language	English
Publishing date	2022-03-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.852812
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Article: Beth Levine's Legacy: From the Discovery of BECN1 to Therapies. A Mentees' Perspective.

An, Zhenyi / Chiang, Wei-Chung / Fernández, Álvaro F / Franco, Luis H / He, CongCong / Huang, Shu-Yi / Lee, Eunmyong / Liu, Yang / Sebti, Salwa / Shoji-Kawata, Sanae / Sirasanagandla, Shyam / Wang, Richard C / Wei, Yongjie / Zhao, Yuting / Vega-Rubin-de-Celis, Silvia

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 891332

Abstract: With great sadness, the scientific community received the news of the loss of Beth Levine on 15 June 2020. Dr. Levine was a pioneer in the autophagy field and work in her lab led not only to a better understanding of the molecular mechanisms regulating ... ...

Abstract	With great sadness, the scientific community received the news of the loss of Beth Levine on 15 June 2020. Dr. Levine was a pioneer in the autophagy field and work in her lab led not only to a better understanding of the molecular mechanisms regulating the pathway, but also its implications in multiple physiological and pathological conditions, including its role in development, host defense, tumorigenesis, aging or metabolism. This review does not aim to provide a comprehensive view of autophagy, but rather an outline of some of the discoveries made by the group of Beth Levine, from the perspective of some of her own mentees, hoping to honor her legacy in science.
Language	English
Publishing date	2022-06-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.891332
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Article ; Online: Broad-Spectrum HDAC Inhibitors Promote Autophagy through FOXO Transcription Factors in Neuroblastoma.

Körholz, Katharina / Ridinger, Johannes / Krunic, Damir / Najafi, Sara / Gerloff, Xenia F / Frese, Karen / Meder, Benjamin / Peterziel, Heike / Vega-Rubin-de-Celis, Silvia / Witt, Olaf / Oehme, Ina

Cells

2021 Volume 10, Issue 5

Abstract: Depending on context and tumor stage, deregulation of autophagy can either suppress tumorigenesis or promote chemoresistance and tumor survival. Histone deacetylases (HDACs) can modulate autophagy; however, the exact mechanisms are not fully understood. ... ...

Abstract	Depending on context and tumor stage, deregulation of autophagy can either suppress tumorigenesis or promote chemoresistance and tumor survival. Histone deacetylases (HDACs) can modulate autophagy; however, the exact mechanisms are not fully understood. Here, we analyze the effects of the broad-spectrum HDAC inhibitors (HDACi) panobinostat and vorinostat on the transcriptional regulation of autophagy with respect to autophagy transcription factor activity (Transcription factor EB-TFEB, forkhead boxO-FOXO) and autophagic flux in neuroblastoma cells. In combination with the late-stage autophagic flux inhibitor bafilomycin A1, HDACis increase the number of autophagic vesicles, indicating an increase in autophagic flux. Both HDACi induce nuclear translocation of the transcription factors FOXO1 and FOXO3a, but not TFEB and promote the expression of pro-autophagic FOXO1/3a target genes. Moreover, FOXO1/3a knockdown experiments impaired HDACi treatment mediated expression of autophagy related genes. Combination of panobinostat with the lysosomal inhibitor chloroquine, which blocks autophagic flux, enhances neuroblastoma cell death in culture and hampers tumor growth in vivo in a neuroblastoma zebrafish xenograft model. In conclusion, our results indicate that pan-HDACi treatment induces autophagy in neuroblastoma at a transcriptional level. Combining HDACis with autophagy modulating drugs suppresses tumor growth of high-risk neuroblastoma cells. These experimental data provide novel insights for optimization of treatment strategies in neuroblastoma.
MeSH term(s)	Animals ; Antimalarials/pharmacology ; Autophagy ; Chloroquine/pharmacology ; Forkhead Box Protein O1/genetics ; Forkhead Box Protein O1/metabolism ; Forkhead Box Protein O3/genetics ; Forkhead Box Protein O3/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Mechanistic Target of Rapamycin Complex 1/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Neuroblastoma/drug therapy ; Neuroblastoma/metabolism ; Neuroblastoma/pathology ; Tumor Cells, Cultured ; Vorinostat/pharmacology ; Xenograft Model Antitumor Assays ; Zebrafish
Chemical Substances	Antimalarials ; FOXO1 protein, human ; FOXO3 protein, human ; Forkhead Box Protein O1 ; Forkhead Box Protein O3 ; Histone Deacetylase Inhibitors ; Vorinostat (58IFB293JI) ; Chloroquine (886U3H6UFF) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2021-04-24
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10051001
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