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Article: The Role of the Ectopeptidase APN/CD13 in Cancer.

Lendeckel, Uwe / Karimi, Farzaneh / Al Abdulla, Ruba / Wolke, Carmen

2023 Volume 11, Issue 3

Abstract: APN/CD13 is expressed in a variety of cells/tissues and is therefore associated with diverse physiological functions, including proliferation, differentiation, migration, angiogenesis, invasion, metastasis, vasoconstriction, and the regulation of normal ... ...

Abstract	APN/CD13 is expressed in a variety of cells/tissues and is therefore associated with diverse physiological functions, including proliferation, differentiation, migration, angiogenesis, invasion, metastasis, vasoconstriction, and the regulation of normal and impaired immune function. Increased expression or activity of APN/CD13 has been described for various tumors, such that APN/CD13 is in most cases associated with reduced disease-free and overall survival. The mechanisms that mediate these cellular effects of APN/CD13 have been largely determined and are described here. APN/CD13-regulated signaling pathways include integrin recycling, the regulation of small GTPase activities, cell-ECM interactions, and Erk1/2, PI3K, and Wnt signaling. APN/CD13 is a neo-angiogenesis marker that is not found on normal endothelia, but it is found on neo-angiogenetically active endothelia. Therefore, APN/CD13 represents a specific receptor for so-called "tumor-homing peptides" (NRG peptides). Peptides containing the NRG motif show high-affinity binding to APN/CD13. APN/CD13 thus represents a versatile target for the inhibition of tumor-induced angiogenesis through the tumor-selective administration of, e.g., cytotoxic substances. Furthermore, it enables the molecular imaging of tumor masses and the assessment of (neo)angiogenesis in animal models and in patients. Pharmacological inhibitors of APN/CD13 have been proven to reduce tumor growth and tumor progression in various APN/CD13-positive tumors.
Language	English
Publishing date	2023-02-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11030724
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Article ; Online: Screening of Relevant Metabolism-Disrupting Chemicals on Pancreatic β-Cells: Evaluation of Murine and Human In Vitro Models.

Al-Abdulla, Ruba / Ferrero, Hilda / Soriano, Sergi / Boronat-Belda, Talía / Alonso-Magdalena, Paloma

International journal of molecular sciences

2022 Volume 23, Issue 8

Abstract: Endocrine-disrupting chemicals (EDCs) are chemical substances that can interfere with the normal function of the endocrine system. EDCs are ubiquitous and can be found in a variety of consumer products such as food packaging materials, personal care and ... ...

Abstract	Endocrine-disrupting chemicals (EDCs) are chemical substances that can interfere with the normal function of the endocrine system. EDCs are ubiquitous and can be found in a variety of consumer products such as food packaging materials, personal care and household products, plastic additives, and flame retardants. Over the last decade, the impact of EDCs on human health has been widely acknowledged as they have been associated with different endocrine diseases. Among them, a subset called metabolism-disrupting chemicals (MDCs) is able to promote metabolic changes that can lead to the development of metabolic disorders such as diabetes, obesity, hepatic steatosis, and metabolic syndrome, among others. Despite this, today, there are still no definitive and standardized in vitro tools to support the metabolic risk assessment of existing and emerging MDCs for regulatory purposes. Here, we evaluated the following two different pancreatic cell-based in vitro systems: the murine pancreatic β-cell line MIN6 as well as the human pancreatic β-cell line EndoC-βH1. Both were challenged with the following range of relevant concentrations of seven well-known EDCs: (bisphenol-A (BPA), bisphenol-S (BPS), bisphenol-F (BPF), perfluorooctanesulfonic acid (PFOS), di(2-ethylhexyl) phthalate (DEHP), cadmium chloride (CdCl
MeSH term(s)	Animals ; Benzhydryl Compounds ; Dichlorodiphenyl Dichloroethylene ; Endocrine Disruptors/toxicity ; Humans ; Insulin ; Mice ; Plastics
Chemical Substances	Benzhydryl Compounds ; Endocrine Disruptors ; Insulin ; Plastics ; Dichlorodiphenyl Dichloroethylene (4M7FS82U08)
Language	English
Publishing date	2022-04-10
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/ijms23084182
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Article ; Online: Exploring the Effects of Metabolism-Disrupting Chemicals on Pancreatic α-Cell Viability, Gene Expression and Function: A Screening Testing Approach.

Al-Abdulla, Ruba / Ferrero, Hilda / Boronat-Belda, Talía / Soriano, Sergi / Quesada, Iván / Alonso-Magdalena, Paloma

International journal of molecular sciences

2023 Volume 24, Issue 2

Abstract: Humans are constantly exposed to many environmental pollutants, some of which have been largely acknowledged as key factors in the development of metabolic disorders such as diabetes and obesity. These chemicals have been classified as endocrine- ... ...

Abstract	Humans are constantly exposed to many environmental pollutants, some of which have been largely acknowledged as key factors in the development of metabolic disorders such as diabetes and obesity. These chemicals have been classified as endocrine-disrupting chemicals (EDCs) and, more recently, since they can interfere with metabolic functions, they have been renamed as metabolism-disrupting chemicals (MDCs). MDCs are present in many consumer products, including food packaging, personal care products, plastic bottles and containers, and detergents. The scientific literature has ever-increasingly focused on insulin-releasing pancreatic β-cells as one of the main targets for MDCs. Evidence highlights that these substances may disrupt glucose homeostasis by altering pancreatic β-cell physiology. However, their potential impact on glucagon-secreting pancreatic α-cells remains poorly known despite the essential role that this cellular type plays in controlling glucose metabolism. In the present study, we have selected seven paradigmatic MDCs representing major toxic classes, including bisphenols, phthalates, perfluorinated compounds, metals, and pesticides. By using an in vitro cell-based model, the pancreatic α-cell line αTC1-9, we have explored the effects of these compounds on pancreatic α-cell viability, gene expression, and secretion. We found that cell viability was moderately affected after bisphenol-A (BPA), bisphenol-F (BPF), and perfluorooctanesulfonic acid (PFOS) exposure, although cytotoxicity was relatively low. In addition, all bisphenols, as well as di(2-ethylhexyl) phthalate (DEHP) and cadmium chloride (CdCl
MeSH term(s)	Humans ; Glucagon ; Cell Survival ; Environmental Pollutants/toxicity ; Insulin ; Benzhydryl Compounds/toxicity ; Endocrine Disruptors/toxicity ; Gene Expression
Chemical Substances	Glucagon (9007-92-5) ; Environmental Pollutants ; Insulin ; Benzhydryl Compounds ; bisphenol A (MLT3645I99) ; Endocrine Disruptors
Language	English
Publishing date	2023-01-05
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/ijms24021044
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Article ; Online: Immunogenic cell death triggered by impaired deubiquitination in multiple myeloma relies on dysregulated type I interferon signaling.

Waad Sadiq, Zeinab / Brioli, Annamaria / Al-Abdulla, Ruba / Çetin, Gonca / Schütt, Jacqueline / Murua Escobar, Hugo / Krüger, Elke / Ebstein, Frédéric

Frontiers in immunology

2023 Volume 14, Page(s) 982720

Abstract: Introduction: Proteasome inhibition is first line therapy in multiple myeloma (MM). The immunological potential of cell death triggered by defects of the ubiquitin-proteasome system (UPS) and subsequent perturbations of protein homeostasis is, however, ... ...

Abstract	Introduction: Proteasome inhibition is first line therapy in multiple myeloma (MM). The immunological potential of cell death triggered by defects of the ubiquitin-proteasome system (UPS) and subsequent perturbations of protein homeostasis is, however, less well defined. Methods: In this paper, we applied the protein homeostasis disruptors bortezomib (BTZ), ONX0914, RA190 and PR619 to various MM cell lines and primary patient samples to investigate their ability to induce immunogenic cell death (ICD). Results: Our data show that while BTZ treatment triggers sterile type I interferon (IFN) responses, exposure of the cells to ONX0914 or RA190 was mostly immunologically silent. Interestingly, inhibition of protein de-ubiquitination by PR619 was associated with the acquisition of a strong type I IFN gene signature which relied on key components of the unfolded protein and integrated stress responses including inositol-requiring enzyme 1 (IRE1), protein kinase R (PKR) and general control nonderepressible 2 (GCN2). The immunological relevance of blocking de-ubiquitination in MM was further reflected by the ability of PR619-induced apoptotic cells to facilitate dendritic cell (DC) maturation Conclusion: Altogether, our findings identify de-ubiquitination inhibition as a promising strategy for inducing ICD of MM to expand current available treatments.
MeSH term(s)	Humans ; Multiple Myeloma/metabolism ; Proteasome Inhibitors/pharmacology ; Proteasome Endopeptidase Complex/metabolism ; Immunogenic Cell Death ; Bortezomib/pharmacology ; Interferon Type I
Chemical Substances	RA190 ; Proteasome Inhibitors ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Bortezomib (69G8BD63PP) ; Interferon Type I
Language	English
Publishing date	2023-03-02
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.982720
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Article ; Online: Role of organic cation transporter 3 (OCT3) in the response of hepatocellular carcinoma to tyrosine kinase inhibitors.

Herraez, Elisa / Al-Abdulla, Ruba / Soto, Meraris / Briz, Oscar / Bettinger, Dominik / Bantel, Heike / Del Carmen, Sofia / Serrano, Maria A / Geier, Andreas / Marin, Jose J G / Macias, Rocio I R

Biochemical pharmacology

2023 Volume 217, Page(s) 115812

Abstract: Impaired function of organic cation transporter 1 (OCT1) in hepatocellular carcinoma (HCC) has been associated with unsatisfactory response to sorafenib. However, some patients lacking OCT1 at the plasma membrane (PM) of HCC cells still respond to ... ...

Abstract	Impaired function of organic cation transporter 1 (OCT1) in hepatocellular carcinoma (HCC) has been associated with unsatisfactory response to sorafenib. However, some patients lacking OCT1 at the plasma membrane (PM) of HCC cells still respond to sorafenib, suggesting that another transporter may contribute to take up this drug. The aim of this study was to investigate whether OCT3 could contribute to the uptake of sorafenib and other tyrosine kinase inhibitors (TKIs) and whether OCT3 determination can predict HCC response to sorafenib. Cells overexpressing OCT3 were used to determine the ability of this carrier to transport sorafenib. Immunostaining of OCT3 was performed in HCC samples obtained in the TRANSFER study. Considering the intensity of staining and the number of OCT3-positive cells, tumors were classified as having absent, weak, moderate, or strong OCT3 expression and were also categorized according to the presence or absence of PM staining. Functional in vitro studies revealed that OCT3 is also able to mediate sorafenib uptake. Other TKIs, such as regorafenib, lenvatinib, and cabozantinib can also interact with this transporter. In silico studies suggested that the expression of OCT3 is better preserved in HCC than that of OCT1. In HCC samples, OCT3 was expressed at the PM of cancer cells, and its presence, detected in 26% of tumors, was associated with better outcomes in patients treated with sorafenib. In conclusion, analysis by immunohistochemistry of OCT3 in the PM of tumor cells may help to predict the response of HCC patients to sorafenib and potentially to other TKIs.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular/metabolism ; Liver Neoplasms/metabolism ; Membrane Transport Proteins ; Sorafenib/pharmacology ; Sorafenib/therapeutic use ; Tyrosine Kinase Inhibitors
Chemical Substances	Membrane Transport Proteins ; Sorafenib (9ZOQ3TZI87) ; Tyrosine Kinase Inhibitors
Language	English
Publishing date	2023-09-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2023.115812
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Article ; Online: Bisphenol-A exposure during pregnancy alters pancreatic β-cell division and mass in male mice offspring: A role for ERβ.

Boronat-Belda, Talía / Ferrero, Hilda / Al-Abdulla, Ruba / Quesada, Iván / Gustafsson, Jan-Ake / Nadal, Ángel / Alonso-Magdalena, Paloma

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

2020 Volume 145, Page(s) 111681

Abstract: Bisphenol-A (BPA) is a widespread endocrine disrupting chemical that constitutes a risk factor for type 2 diabetes mellitus (T2DM). Data from animal and human studies have demonstrated that early exposure to BPA results in adverse metabolic outcomes in ... ...

Abstract	Bisphenol-A (BPA) is a widespread endocrine disrupting chemical that constitutes a risk factor for type 2 diabetes mellitus (T2DM). Data from animal and human studies have demonstrated that early exposure to BPA results in adverse metabolic outcomes in adult life. In the present work, we exposed pregnant heterozygous estrogen receptor β (ERβ) knock out (BERKO) mice to 10 μg/kg/day BPA, during days 9-16 of pregnancy, and measured β-cell mass and proliferation in wildtype (WT) and BERKO male offspring at postnatal day 30. We observed increased pancreatic β-cell proliferation and mass in WT, yet no effect was produced in BERKO mice. Dispersed islet cells in primary culture treated with 1 nM BPA showed an enhanced pancreatic β-cell replication rate, which was blunted in pancreatic β-cells from BERKO mice and mimicked by the selective ERβ agonist WAY200070. This increased β-cell proliferation was found in male adult as well as in neonate pancreatic β-cells, suggesting that BPA directly impacts β-cell division at earliest stages of life. These findings strongly indicate that BPA during pregnancy upregulates pancreatic β-cell division and mass in an ERβ-dependent manner. Thus, other natural or artificial chemicals may use this ERβ-mediated pathway to promote similar effects.
MeSH term(s)	Animals ; Benzhydryl Compounds/toxicity ; Cell Division/drug effects ; Cell Proliferation/drug effects ; Estrogen Receptor beta/genetics ; Estrogen Receptor beta/metabolism ; Female ; Humans ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Male ; Maternal Exposure/adverse effects ; Mice ; Mice, Knockout ; Phenols/toxicity ; Pregnancy ; Prenatal Exposure Delayed Effects/etiology ; Prenatal Exposure Delayed Effects/genetics ; Prenatal Exposure Delayed Effects/metabolism
Chemical Substances	Benzhydryl Compounds ; Estrogen Receptor beta ; Phenols ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2020-08-14
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.2020.111681
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Article ; Online: Unraveling 'The Cancer Genome Atlas' information on the role of SLC transporters in anticancer drug uptake.

Al-Abdulla, Ruba / Perez-Silva, Laura / Abete, Lorena / Romero, Marta R / Briz, Oscar / Marin, Jose J G

Expert review of clinical pharmacology

2019 Volume 12, Issue 4, Page(s) 329–341

Abstract: Introduction: Anticancer chemotherapy often faces the problem of intrinsic or acquired drug refractoriness due in part to efficient mechanisms of defense present or developed, respectively, in cancer cells. Owing to their polarity and/or high molecular ... ...

Abstract	Introduction: Anticancer chemotherapy often faces the problem of intrinsic or acquired drug refractoriness due in part to efficient mechanisms of defense present or developed, respectively, in cancer cells. Owing to their polarity and/or high molecular weight, many cytostatic agents cannot freely cross the plasma membrane by simple diffusion and hence depend on SLC proteins to enter cancer cells. The downregulation of these transporters and the appearance of either inactivating mutations or aberrant splicing, hamper the possibility of anticancer drugs to interact with their intracellular targets. Areas covered: In addition to specific literature, we have revised Gene database of the NCBI PubMed resources and information publicly available at NIH 'The Cancer Genome Atlas' (TCGA) (update November 2018) to evaluate the relationship between the profile of expression of SLC transporters playing a major role in the transportome and accounting for drug uptake, in healthy and tumor tissue, and their ability to recognize as substrate several antitumor drugs frequently used in the treatment of different types of cancer, which could affect the overall response to chemotherapy based on regimens including these drugs. Expert commentary: Changes in the transportome may affect the overall response to chemotherapy based on drugs taken up by SLC transporters.
MeSH term(s)	Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/pharmacokinetics ; Biological Transport ; Genome, Human ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Solute Carrier Proteins/genetics ; Solute Carrier Proteins/metabolism ; Tissue Distribution ; Treatment Outcome
Chemical Substances	Antineoplastic Agents ; Solute Carrier Proteins
Language	English
Publishing date	2019-02-26
Publishing country	England
Document type	Journal Article ; Review
ISSN	1751-2441
ISSN (online)	1751-2441
DOI	10.1080/17512433.2019.1581605
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Article ; Online: What "The Cancer Genome Atlas" database tells us about the role of ATP-binding cassette (ABC) proteins in chemoresistance to anticancer drugs.

Briz, Oscar / Perez-Silva, Laura / Al-Abdulla, Ruba / Abete, Lorena / Reviejo, Maria / Romero, Marta R / Marin, Jose J G

Expert opinion on drug metabolism & toxicology

2019 Volume 15, Issue 7, Page(s) 577–593

Abstract: ... ...

Abstract	Introduction
MeSH term(s)	ATP-Binding Cassette Transporters/genetics ; ATP-Binding Cassette Transporters/metabolism ; Antineoplastic Agents/pharmacology ; Databases, Genetic ; Drug Resistance, Neoplasm/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Up-Regulation
Chemical Substances	ATP-Binding Cassette Transporters ; Antineoplastic Agents
Language	English
Publishing date	2019-06-23
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2214462-6
ISSN	1744-7607 ; 1742-5255
ISSN (online)	1744-7607
ISSN	1742-5255
DOI	10.1080/17425255.2019.1631285
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Article ; Online: Fibroblast-Derived Lysyl Oxidase Increases Oxidative Phosphorylation and Stemness in Cholangiocarcinoma.

Gastroenterology

2023 Volume 166, Issue 5, Page(s) 886–901.e7

Abstract: Background & aims: Metabolic and transcriptional programs respond to extracellular matrix-derived cues in complex environments, such as the tumor microenvironment. Here, we demonstrate how lysyl oxidase (LOX), a known factor in collagen crosslinking, ... ...

Abstract	Background & aims: Metabolic and transcriptional programs respond to extracellular matrix-derived cues in complex environments, such as the tumor microenvironment. Here, we demonstrate how lysyl oxidase (LOX), a known factor in collagen crosslinking, contributes to the development and progression of cholangiocarcinoma (CCA). Methods: Transcriptomes of 209 human CCA tumors, 143 surrounding tissues, and single-cell data from 30 patients were analyzed. The recombinant protein and a small molecule inhibitor of the LOX activity were used on primary patient-derived CCA cultures to establish the role of LOX in migration, proliferation, colony formation, metabolic fitness, and the LOX interactome. The oncogenic role of LOX was further investigated by RNAscope and in vivo using the AKT/NICD genetically engineered murine CCA model. Results: We traced LOX expression to hepatic stellate cells and specifically hepatic stellate cell-derived inflammatory cancer-associated fibroblasts and found that cancer-associated fibroblast-driven LOX increases oxidative phosphorylation and metabolic fitness of CCA, and regulates mitochondrial function through transcription factor A, mitochondrial. Inhibiting LOX activity in vivo impedes CCA development and progression. Our work highlights that LOX alters tumor microenvironment-directed transcriptional reprogramming of CCA cells by facilitating the expression of the oxidative phosphorylation pathway and by increasing stemness and mobility. Conclusions: Increased LOX is driven by stromal inflammatory cancer-associated fibroblasts and correlates with diminished survival of patients with CCA. Modulating the LOX activity can serve as a novel tumor microenvironment-directed therapeutic strategy in bile duct pathologies.
MeSH term(s)	Cholangiocarcinoma/pathology ; Cholangiocarcinoma/metabolism ; Cholangiocarcinoma/genetics ; Cholangiocarcinoma/enzymology ; Humans ; Protein-Lysine 6-Oxidase/metabolism ; Protein-Lysine 6-Oxidase/genetics ; Bile Duct Neoplasms/pathology ; Bile Duct Neoplasms/metabolism ; Bile Duct Neoplasms/genetics ; Bile Duct Neoplasms/enzymology ; Animals ; Tumor Microenvironment ; Oxidative Phosphorylation ; Mice ; Cancer-Associated Fibroblasts/metabolism ; Cancer-Associated Fibroblasts/pathology ; Cancer-Associated Fibroblasts/enzymology ; Hepatic Stellate Cells/metabolism ; Hepatic Stellate Cells/pathology ; Hepatic Stellate Cells/enzymology ; Neoplastic Stem Cells/pathology ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/enzymology ; Cell Proliferation ; Cell Movement ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Signal Transduction
Chemical Substances	Protein-Lysine 6-Oxidase (EC 1.4.3.13) ; LOX protein, human (EC 1.4.3.13)
Language	English
Publishing date	2023-12-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2023.11.302
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Article ; Online: Relationship between changes in the exon-recognition machinery and SLC22A1 alternative splicing in hepatocellular carcinoma.

Soto, Meraris / Reviejo, Maria / Al-Abdulla, Ruba / Romero, Marta R / Macias, Rocio I R / Boix, Loreto / Bruix, Jordi / Serrano, Maria A / Marin, Jose J G

Biochimica et biophysica acta. Molecular basis of disease

2020 Volume 1866, Issue 5, Page(s) 165687

Abstract: Changes in the phenotype that characterizes cancer cells are partly due to altered processing of pre-mRNA by the spliceosome. We have previously reported that aberrant splicing plays an essential role in the impaired response of hepatocellular carcinoma ( ...

Abstract	Changes in the phenotype that characterizes cancer cells are partly due to altered processing of pre-mRNA by the spliceosome. We have previously reported that aberrant splicing plays an essential role in the impaired response of hepatocellular carcinoma (HCC) to sorafenib by reducing the expression of functional organic cation transporter type 1 (OCT1, gene SLC22A1) that constitutes the primary way for HCC cells to take up this and other drugs. The present study includes an in silico analysis of publicly available databases to investigate the relationship between alternative splicing of SLC22A1 pre-mRNA and the expression of genes involved in the exon-recognition machinery in HCC and adjacent non-tumor tissue. Using Taqman Low-Density Arrays, the findings were validated in 25 tumors that were resected without neoadjuvant chemotherapy. The results supported previous reports showing that there was a considerable degree of alternative splicing of SLC22A1 in adjacent non-tumor tissue, which was further increased in the tumor in a stage-unrelated manner. Splicing perturbation was associated with changes in the profile of proteins determining exon recognition. The results revealed the importance of using paired samples for splicing analysis in HCC and confirmed that aberrant splicing plays an essential role in the expression of functional OCT1. Changes in the exon recognition machinery may also affect the expression of other proteins in HCC. Moreover, these results pave the way to further investigations on the mechanistic bases of the relationship between the expression of spliceosome-associated genes and its repercussion on the appearance of alternative and aberrant splicing in HCC.
MeSH term(s)	Aged ; Aged, 80 and over ; Alternative Splicing ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/mortality ; Carcinoma, Hepatocellular/pathology ; Computer Simulation ; Datasets as Topic ; Exons/genetics ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Kaplan-Meier Estimate ; Liver/pathology ; Liver Neoplasms/genetics ; Liver Neoplasms/mortality ; Liver Neoplasms/pathology ; Male ; Middle Aged ; Organic Cation Transporter 1/genetics ; RNA Precursors/genetics ; RNA Precursors/metabolism ; Spliceosomes/metabolism
Chemical Substances	Organic Cation Transporter 1 ; RNA Precursors
Language	English
Publishing date	2020-01-15
Publishing country	Netherlands
Document type	Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2020.165687
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