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Article ; Online: Sprouty1 is a broad mediator of cellular senescence.

Anerillas, Carlos / Perramon-Güell, Aida / Altés, Gisela / Cuesta, Sara / Vaquero, Marta / Olomí, Anna / Rodríguez-Barrueco, Ruth / Llobet-Navàs, David / Egea, Joaquim / Dolcet, Xavi / Yeramian, Andrée / Encinas, Mario

Cell death & disease

2024 Volume 15, Issue 4, Page(s) 296

Abstract: Genes of the Sprouty family (Spry1-4) restrain signaling by certain receptor tyrosine kinases. Consequently, these genes participate in several developmental processes and function as tumor suppressors in adult life. Despite these important roles, the ... ...

Abstract	Genes of the Sprouty family (Spry1-4) restrain signaling by certain receptor tyrosine kinases. Consequently, these genes participate in several developmental processes and function as tumor suppressors in adult life. Despite these important roles, the biology of this family of genes still remains obscure. Here we show that Sprouty proteins are general mediators of cellular senescence. Induction of cellular senescence by several triggers in vitro correlates with upregulation of Sprouty protein levels. More importantly, overexpression of Sprouty genes is sufficient to cause premature cellular senescence, via a conserved N-terminal tyrosine (Tyrosine 53 of Sprouty1). Accordingly, fibroblasts from knockin animals lacking that tyrosine escape replicative senescence. In vivo, heterozygous knockin mice display delayed induction of cellular senescence during cutaneous wound healing and upon chemotherapy-induced cellular senescence. Unlike other functions of this family of genes, induction of cellular senescence appears to be independent of activation of the ERK1/2 pathway. Instead, we show that Sprouty proteins induce cellular senescence upstream of the p38 pathway in these in vitro and in vivo paradigms.
MeSH term(s)	Cellular Senescence ; Animals ; Mice ; Membrane Proteins/metabolism ; Membrane Proteins/genetics ; Humans ; Fibroblasts/metabolism ; Adaptor Proteins, Signal Transducing/metabolism ; Adaptor Proteins, Signal Transducing/genetics ; Phosphoproteins/metabolism ; Phosphoproteins/genetics ; p38 Mitogen-Activated Protein Kinases/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Intracellular Signaling Peptides and Proteins/genetics ; MAP Kinase Signaling System ; Wound Healing
Chemical Substances	Membrane Proteins ; Spry1 protein, mouse ; Adaptor Proteins, Signal Transducing ; Phosphoproteins ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Intracellular Signaling Peptides and Proteins ; SPRY1 protein, human
Language	English
Publishing date	2024-04-26
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/s41419-024-06689-4
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Article ; Online: Autophagy in the physiological endometrium and cancer.

Devis-Jauregui, Laura / Eritja, Núria / Davis, Meredith Leigh / Matias-Guiu, Xavier / Llobet-Navàs, David

Autophagy

2020 Volume 17, Issue 5, Page(s) 1077–1095

Abstract: Autophagy is a highly conserved catabolic process and a major cellular pathway for the degradation of long-lived proteins and cytoplasmic organelles. An increasing body of evidence has unveiled autophagy as an indispensable biological function that helps ...

Abstract	Autophagy is a highly conserved catabolic process and a major cellular pathway for the degradation of long-lived proteins and cytoplasmic organelles. An increasing body of evidence has unveiled autophagy as an indispensable biological function that helps to maintain normal tissue homeostasis and metabolic fitness that can also lead to severe consequences for the normal cellular functioning when altered. Recent accumulating data point to autophagy as a key player in a wide variety of physiological and pathophysiological conditions in the human endometrium, one of the most proficient self-regenerating tissues in the human body and an instrumental player in placental species reproductive function. The current review highlights the most recent findings regarding the process of autophagy in the normal and cancerous endometrial tissue. Current research efforts aiming to therapeutically exploit autophagy and the methodological approaches used are discussed.
MeSH term(s)	Apoptosis Regulatory Proteins/metabolism ; Autophagy/physiology ; Endometrium/metabolism ; Female ; Humans ; Hyperplasia/metabolism ; Neoplasms/metabolism ; Placenta/metabolism ; Pregnancy
Chemical Substances	Apoptosis Regulatory Proteins
Language	English
Publishing date	2020-05-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2020.1752548
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Article ; Online: Transient and DNA-free in vivo CRISPR/Cas9 genome editing for flexible modeling of endometrial carcinogenesis.

Navaridas, Raúl / Vidal-Sabanés, Maria / Ruiz-Mitjana, Anna / Perramon-Güell, Aida / Megino-Luque, Cristina / Llobet-Navas, David / Matias-Guiu, Xavier / Egea, Joaquim / Encinas, Mario / Bardia, Lídia / Colombelli, Julien / Dolcet, Xavier

Cancer communications (London, England)

2023 Volume 43, Issue 5, Page(s) 620–624

MeSH term(s)	Humans ; Gene Editing ; CRISPR-Cas Systems ; DNA
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2023-02-10
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ISSN	2523-3548
ISSN (online)	2523-3548
DOI	10.1002/cac2.12409
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Article: Metabolomic Analysis Points to Bioactive Lipid Species and Acireductone Dioxygenase 1 (ADI1) as Potential Therapeutic Targets in Poor Prognosis Endometrial Cancer.

Gatius, Sònia / Jove, Mariona / Megino-Luque, Cristina / Albertí-Valls, Manel / Yeramian, Andree / Bonifaci, Nuria / Piñol, Miquel / Santacana, Maria / Pradas, Irene / Llobet-Navas, David / Pamplona, Reinald / Matías-Guiu, Xavier / Eritja, Núria

Cancers

2022 Volume 14, Issue 12

Abstract: Metabolomic profiling analysis has the potential to highlight new molecules and cellular pathways that may serve as potential therapeutic targets for disease treatment. In this study, we used an LC-MS/MS platform to define, for the first time, the ... ...

Abstract	Metabolomic profiling analysis has the potential to highlight new molecules and cellular pathways that may serve as potential therapeutic targets for disease treatment. In this study, we used an LC-MS/MS platform to define, for the first time, the specific metabolomic signature of uterine serous carcinoma (SC), a relatively rare and aggressive variant of endometrial cancer (EC) responsible for 40% of all endometrial cancer-related deaths. A metabolomic analysis of 31 ECs (20 endometrial endometrioid carcinomas (EECs) and 11 SCs) was performed. Following multivariate statistical analysis, we identified 232 statistically different metabolites among the SC and EEC patient samples. Notably, most of the metabolites identified (89.2%) were lipid species and showed lower levels in SCs when compared to EECs. In addition to lipids, we also documented metabolites belonging to amino acids and purine nucleotides (such as 2-Oxo-4-methylthiobutanoic acid, synthesised by acireductone dioxygenase 1 (ADI1) enzyme), which showed higher levels in SCs. To further investigate the role of ADI1 in SC, we analysed the expression protein levels of ADI1 in 96 ECs (67 EECs and 29 SCs), proving that the levels of ADI1 were higher in SCs compared to EECs. We also found that ADI1 mRNA levels were higher in p53 abnormal ECs compared to p53 wild type tumours. Furthermore, elevated ADI1 mRNA levels showed a statistically significant negative correlation with overall survival and progression-free survival among EEC patients. Finally, we tested the ability of ADI1 to induce migration and invasion capabilities in EC cell lines. Altogether, these results suggest that ADI1 could be a potential therapeutic target in poor-prognosis SCs and other Ecs with abnormal p53 expression.
Language	English
Publishing date	2022-06-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14122842
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Article ; Online: A compound directed against S6K1 hampers fat mass expansion and mitigates diet-induced hepatosteatosis.

Lluch, Aina / Veiga, Sonia R / Latorre, Jèssica / Moreno-Navarrete, José M / Bonifaci, Núria / Dien Nguyen, Van / Zhou, You / Höring, Marcus / Liebisch, Gerhard / Olkkonen, Vesa M / Llobet-Navas, David / Thomas, George / Rodríguez-Barrueco, Ruth / Fernández-Real, José M / Kozma, Sara C / Ortega, Francisco J

JCI insight

2022 Volume 7, Issue 14

Abstract: The ribosomal protein S6 kinase 1 (S6K1) is a relevant effector downstream of the mammalian target of rapamycin complex 1 (mTORC1), best known for its role in the control of lipid homeostasis. Consistent with this, mice lacking the S6k1 gene have a ... ...

Abstract	The ribosomal protein S6 kinase 1 (S6K1) is a relevant effector downstream of the mammalian target of rapamycin complex 1 (mTORC1), best known for its role in the control of lipid homeostasis. Consistent with this, mice lacking the S6k1 gene have a defect in their ability to induce the commitment of fat precursor cells to the adipogenic lineage, which contributes to a significant reduction of fat mass. Here, we assess the therapeutic blockage of S6K1 in diet-induced obese mice challenged with LY2584702 tosylate, a specific oral S6K1 inhibitor initially developed for the treatment of solid tumors. We show that diminished S6K1 activity hampers fat mass expansion and ameliorates dyslipidemia and hepatic steatosis, while modifying transcriptome-wide gene expression programs relevant for adipose and liver function. Accordingly, decreased mTORC1 signaling in fat (but increased in the liver) segregated with defective epithelial-mesenchymal transition and the impaired expression of Cd36 (coding for a fatty acid translocase) and Lgals1 (Galectin 1) in both tissues. All these factors combined align with reduced adipocyte size and improved lipidomic signatures in the liver, while hepatic steatosis and hypertriglyceridemia were improved in treatments lasting either 3 months or 6 weeks.
MeSH term(s)	Animals ; Diet ; Fatty Liver/drug therapy ; Fatty Liver/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Ribosomal Protein S6 Kinases, 90-kDa/antagonists & inhibitors ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Ribosomal Protein S6 Kinases, 90-kDa (EC 2.7.11.1) ; Rps6ka1 protein, mouse (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-07-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.150461
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Article ; Online: Structural disruption of BAF chromatin remodeller impairs neuroblastoma metastasis by reverting an invasiveness epigenomic program.

Jiménez, Carlos / Antonelli, Roberta / Nadal-Ribelles, Mariona / Devis-Jauregui, Laura / Latorre, Pablo / Solé, Carme / Masanas, Marc / Molero-Valenzuela, Adrià / Soriano, Aroa / Sánchez de Toledo, Josep / Llobet-Navas, David / Roma, Josep / Posas, Francesc / de Nadal, Eulàlia / Gallego, Soledad / Moreno, Lucas / Segura, Miguel F

Molecular cancer

2022 Volume 21, Issue 1, Page(s) 175

Abstract: Background: Epigenetic programming during development is essential for determining cell lineages, and alterations in this programming contribute to the initiation of embryonal tumour development. In neuroblastoma, neural crest progenitors block their ... ...

Abstract	Background: Epigenetic programming during development is essential for determining cell lineages, and alterations in this programming contribute to the initiation of embryonal tumour development. In neuroblastoma, neural crest progenitors block their course of natural differentiation into sympathoadrenergic cells, leading to the development of aggressive and metastatic paediatric cancer. Research of the epigenetic regulators responsible for oncogenic epigenomic networks is crucial for developing new epigenetic-based therapies against these tumours. Mammalian switch/sucrose non-fermenting (mSWI/SNF) ATP-dependent chromatin remodelling complexes act genome-wide translating epigenetic signals into open chromatin states. The present study aimed to understand the contribution of mSWI/SNF to the oncogenic epigenomes of neuroblastoma and its potential as a therapeutic target. Methods: Functional characterisation of the mSWI/SNF complexes was performed in neuroblastoma cells using proteomic approaches, loss-of-function experiments, transcriptome and chromatin accessibility analyses, and in vitro and in vivo assays. Results: Neuroblastoma cells contain three main mSWI/SNF subtypes, but only BRG1-associated factor (BAF) complex disruption through silencing of its key structural subunits, ARID1A and ARID1B, impairs cell proliferation by promoting cell cycle blockade. Genome-wide chromatin remodelling and transcriptomic analyses revealed that BAF disruption results in the epigenetic repression of an extensive invasiveness-related expression program involving integrins, cadherins, and key mesenchymal regulators, thereby reducing adhesion to the extracellular matrix and the subsequent invasion in vitro and drastically inhibiting the initiation and growth of neuroblastoma metastasis in vivo. Conclusions: We report a novel ATPase-independent role for the BAF complex in maintaining an epigenomic program that allows neuroblastoma invasiveness and metastasis, urging for the development of new BAF pharmacological structural disruptors for therapeutic exploitation in metastatic neuroblastoma.
MeSH term(s)	Animals ; Child ; Chromatin/genetics ; Chromatin Assembly and Disassembly ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; Epigenomics ; Humans ; Mammals/metabolism ; Neuroblastoma/genetics ; Proteomics
Chemical Substances	Chromatin ; Chromosomal Proteins, Non-Histone
Language	English
Publishing date	2022-09-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2091373-4
ISSN	1476-4598 ; 1476-4598
ISSN (online)	1476-4598
ISSN	1476-4598
DOI	10.1186/s12943-022-01643-4
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Article ; Online: miR-424/503 modulates Wnt/β-catenin signaling in the mammary epithelium by targeting LRP6.

Nekritz, Erin A / Rodriguez-Barrueco, Ruth / Yan, Koon-Kiu / Davis, Meredith L / Werner, Rachel L / Devis-Jauregui, Laura / Mukhopadhyay, Partha / Yu, Jiyang / Llobet-Navas, David / Silva, Jose

EMBO reports

2021 Volume 22, Issue 12, Page(s) e53201

Abstract: During the female lifetime, the expansion of the epithelium dictated by the ovarian cycles is supported by a transient increase in the mammary epithelial stem cell population (MaSCs). Notably, activation of Wnt/β-catenin signaling is an important trigger ...

Abstract	During the female lifetime, the expansion of the epithelium dictated by the ovarian cycles is supported by a transient increase in the mammary epithelial stem cell population (MaSCs). Notably, activation of Wnt/β-catenin signaling is an important trigger for MaSC expansion. Here, we report that the miR-424/503 cluster is a modulator of canonical Wnt signaling in the mammary epithelium. We show that mammary tumors of miR-424(322)/503-depleted mice exhibit activated Wnt/β-catenin signaling. Importantly, we show a strong association between miR-424/503 deletion and breast cancers with high levels of Wnt/β-catenin signaling. Moreover, miR-424/503 cluster is required for Wnt-mediated MaSC expansion induced by the ovarian cycles. Lastly, we show that miR-424/503 exerts its function by targeting two binding sites at the 3'UTR of the LRP6 co-receptor and reducing its expression. These results unveil an unknown link between the miR-424/503, regulation of Wnt signaling, MaSC fate, and tumorigenesis.
MeSH term(s)	Animals ; Breast Neoplasms ; Carcinogenesis ; Cell Line, Tumor ; Epithelial Cells/cytology ; Epithelium/metabolism ; Female ; Low Density Lipoprotein Receptor-Related Protein-6/genetics ; Low Density Lipoprotein Receptor-Related Protein-6/metabolism ; Mammary Glands, Animal/cytology ; Menstrual Cycle ; Mice ; MicroRNAs/genetics ; Stem Cells/cytology ; Wnt Signaling Pathway
Chemical Substances	Low Density Lipoprotein Receptor-Related Protein-6 ; Lrp6 protein, mouse ; MIRN424 microRNA, mouse ; MicroRNAs ; Mirn503 microRNA, mouse
Language	English
Publishing date	2021-10-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.15252/embr.202153201
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Zs.A 5433: 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 ; Online: ARID1A-deficient cells require HDAC6 for progression of endometrial carcinoma.

Megino-Luque, Cristina / Sisó, Pol / Mota-Martorell, Natalia / Navaridas, Raúl / de la Rosa, Inés / Urdanibia, Izaskun / Albertí-Valls, Manel / Santacana, Maria / Pinyol, Miquel / Bonifaci, Núria / Macià, Anna / Llobet-Navas, David / Gatius, Sònia / Matias-Guiu, Xavier / Eritja, Núria

Molecular oncology

2022 Volume 16, Issue 11, Page(s) 2235–2259

Abstract: AT-rich interactive domain-containing protein 1A (ARID1A) loss-of-function mutation accompanied by a loss of ARID1A protein expression is frequently observed in endometrial carcinomas. However, the molecular mechanisms linking these genetic changes to ... ...

Abstract	AT-rich interactive domain-containing protein 1A (ARID1A) loss-of-function mutation accompanied by a loss of ARID1A protein expression is frequently observed in endometrial carcinomas. However, the molecular mechanisms linking these genetic changes to the altered pathways regulating tumour initiation, maintenance and/or progression remain poorly understood. Thus, the main aim of this study was to analyse the role of ARID1A loss of function in endometrial tumorigenesis. Here, using different endometrial in vitro and in vivo models, such as tumoral cell lines, 3D primary cultures and metastatic or genetically modified mouse models, we show that altered expression of ARID1A is not enough to initiate endometrial tumorigenesis. However, in an established endometrial cancer context, ARID1A loss of function accelerates tumoral progression and metastasis through the disruption of the G2/M cell cycle checkpoint and ATM/ATR-mediated DNA damage checkpoints, increases epithelial cell proliferation rates and induces epithelial mesenchymal transition through the activation of histone deacetylase 6 (HDAC6). Next, we demonstrated that the inhibition of HDAC6 function, using the HDAC6-specific inhibitor ACY1215 or by transfection with HDAC6 short hairpin RNA (shRNA), can reverse the migratory and invasive phenotype of ARID1A-knockdown cells. Further, we also show that inhibition of HDAC6 activity causes an apoptotic vulnerability to etoposide treatments in ARID1A-deficient cells. In summary, the findings exposed in this work indicate that the inhibition of HDAC6 activity is a potential therapeutic strategy for patients suffering from ARID1A-mutant endometrial cancer diagnosed in advanced stages.
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Cell Proliferation/genetics ; DNA-Binding Proteins/genetics ; Endometrial Neoplasms/genetics ; Endometrial Neoplasms/pathology ; Epithelial-Mesenchymal Transition ; Female ; Histone Deacetylase 6/genetics ; Humans ; Mice ; Transcription Factors/genetics
Chemical Substances	ARID1A protein, human ; Arid1a protein, mouse ; DNA-Binding Proteins ; Transcription Factors ; HDAC6 protein, human (EC 3.5.1.98) ; Hdac6 protein, mouse (EC 3.5.1.98) ; Histone Deacetylase 6 (EC 3.5.1.98)
Language	English
Publishing date	2022-03-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1002/1878-0261.13193
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Article: Neuronal Differentiation-Related Epigenetic Regulator

Jiménez, Carlos / Antonelli, Roberta / Masanas, Marc / Soriano, Aroa / Devis-Jauregui, Laura / Camacho, Jessica / Magdaleno, Ainara / Guillén, Gabriela / Hladun, Raquel / Jubierre, Luz / Roma, Josep / Llobet-Navas, David / Sánchez de Toledo, Josep / Moreno, Lucas / Gallego, Soledad / Segura, Miguel F

Cancers

2021 Volume 13, Issue 19

Abstract: Neuroblastoma is a pediatric tumor of the peripheral nervous system that accounts for up to ~15% of all cancer-related deaths in children. Recently, it has become evident that epigenetic deregulation is a relevant event in pediatric tumors such as high- ... ...

Abstract	Neuroblastoma is a pediatric tumor of the peripheral nervous system that accounts for up to ~15% of all cancer-related deaths in children. Recently, it has become evident that epigenetic deregulation is a relevant event in pediatric tumors such as high-risk neuroblastomas, and a determinant for processes, such as cell differentiation blockade and sustained proliferation, which promote tumor progression and resistance to current therapies. Thus, a better understanding of epigenetic factors implicated in the aggressive behavior of neuroblastoma cells is crucial for the development of better treatments. In this study, we characterized the role of
Language	English
Publishing date	2021-09-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13194845
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Article ; Online: Gasdermin B over-expression modulates HER2-targeted therapy resistance by inducing protective autophagy through Rab7 activation.

Journal of experimental & clinical cancer research : CR

2022 Volume 41, Issue 1, Page(s) 285

Abstract: Background: Gasdermin B (GSDMB) over-expression promotes poor prognosis and aggressive behavior in HER2 breast cancer by increasing resistance to therapy. Decoding the molecular mechanism of GSDMB-mediated drug resistance is crucial to identify novel ... ...

Abstract	Background: Gasdermin B (GSDMB) over-expression promotes poor prognosis and aggressive behavior in HER2 breast cancer by increasing resistance to therapy. Decoding the molecular mechanism of GSDMB-mediated drug resistance is crucial to identify novel effective targeted treatments for HER2/GSDMB aggressive tumors. Methods: Different in vitro approaches (immunoblot, qRT-PCR, flow cytometry, proteomic analysis, immunoprecipitation, and confocal/electron microscopy) were performed in HER2 breast and gastroesophageal carcinoma cell models. Results were then validated using in vivo preclinical animal models and analyzing human breast and gastric cancer samples. Results: GSDMB up-regulation renders HER2 cancer cells more resistant to anti-HER2 agents by promoting protective autophagy. Accordingly, the combination of lapatinib with the autophagy inhibitor chloroquine increases the therapeutic response of GSDMB-positive cancers in vitro and in zebrafish and mice tumor xenograft in vivo models. Mechanistically, GSDMB N-terminal domain interacts with the key components of the autophagy machinery LC3B and Rab7, facilitating the Rab7 activation during pro-survival autophagy in response to anti-HER2 therapies. Finally, we validated these results in clinical samples where GSDMB/Rab7/LC3B co-expression associates significantly with relapse in HER2 breast and gastric cancers. Conclusion: Our findings uncover for the first time a functional link between GSDMB over-expression and protective autophagy in response to HER2-targeted therapies. GSDMB behaves like an autophagy adaptor and plays a pivotal role in modulating autophagosome maturation through Rab7 activation. Finally, our results provide a new and accessible therapeutic approach for HER2/GSDMB + cancers with adverse clinical outcome.
MeSH term(s)	Animals ; Autophagy ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Cell Line, Tumor ; Chloroquine/pharmacology ; Drug Resistance, Neoplasm ; Female ; Humans ; Lapatinib/pharmacology ; Mice ; Neoplasm Recurrence, Local ; Proteomics ; Receptor, ErbB-2/genetics ; Zebrafish
Chemical Substances	Lapatinib (0VUA21238F) ; Chloroquine (886U3H6UFF) ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2022-09-26
Publishing country	England
Document type	Journal Article
ZDB-ID	803138-1
ISSN	1756-9966 ; 0392-9078
ISSN (online)	1756-9966
ISSN	0392-9078
DOI	10.1186/s13046-022-02497-w
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