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Jurcevic, S., Keane, S., Borgmästars, E., Lubovac-Pilav, Z. & Ejeskär, K. (2022). Bioinformatics analysis of miRNAs in the neuroblastoma 11q-deleted region reveals a role of miR-548l in both 11q-deleted and MYCN amplified tumour cells. Scientific Reports, 12(1), Article ID 19729.
Open this publication in new window or tab >>Bioinformatics analysis of miRNAs in the neuroblastoma 11q-deleted region reveals a role of miR-548l in both 11q-deleted and MYCN amplified tumour cells
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2022 (English)In: Scientific Reports, E-ISSN 2045-2322, Vol. 12, no 1, article id 19729Article in journal (Refereed) Published
Abstract [en]

Neuroblastoma is a childhood tumour that is responsible for approximately 15% of all childhood cancer deaths. Neuroblastoma tumours with amplification of the oncogene MYCN are aggressive, however, another aggressive subgroup without MYCN amplification also exists; rather, they have a deleted region at chromosome arm 11q. Twenty-six miRNAs are located within the breakpoint region of chromosome 11q and have been checked for a possible involvement in development of neuroblastoma due to the genomic alteration. Target genes of these miRNAs are involved in pathways associated with cancer, including proliferation, apoptosis and DNA repair. We could show that miR-548l found within the 11q region is downregulated in neuroblastoma cell lines with 11q deletion or MYCN amplification. In addition, we showed that the restoration of miR-548l level in a neuroblastoma cell line led to a decreased proliferation of these cells as well as a decrease in the percentage of cells in the S phase. We also found that miR-548l overexpression suppressed cell viability and promoted apoptosis, while miR-548l knockdown promoted cell viability and inhibited apoptosis in neuroblastoma cells. Our results indicate that 11q-deleted neuroblastoma and MYCN amplified neuroblastoma coalesce by downregulating miR-548l.

Place, publisher, year, edition, pages
Springer Nature, 2022
National Category
Bioinformatics and Systems Biology Biomedical Laboratory Science/Technology Bioinformatics (Computational Biology) Cancer and Oncology Medical Genetics Cell and Molecular Biology
Research subject
Infection Biology; Translational Medicine TRIM; Bioinformatics
Identifiers
urn:nbn:se:his:diva-22068 (URN)10.1038/s41598-022-24140-6 (DOI)000885172100065 ()36396668 (PubMedID)2-s2.0-85142197814 (Scopus ID)
Funder
Swedish Childhood Cancer Foundation
Note

CC BY 4.0

© 2022 Springer Nature Limited

We thank the Swedish Childhood Cancer Fund and Assar Gabrielsson Found for financial support.

Open access funding provided by University of Skövde.

Correspondence and requests for materials should be addressed to S.J.

Available from: 2022-11-21 Created: 2022-11-21 Last updated: 2023-01-16Bibliographically approved
Keane, S., de Weerd, H. A. & Ejeskär, K. (2022). DLG2 impairs dsDNA break repair and maintains genome integrity in neuroblastoma. DNA Repair, 112, Article ID 103302.
Open this publication in new window or tab >>DLG2 impairs dsDNA break repair and maintains genome integrity in neuroblastoma
2022 (English)In: DNA Repair, ISSN 1568-7864, E-ISSN 1568-7856, Vol. 112, article id 103302Article in journal (Refereed) Published
Abstract [en]

Background

In primary neuroblastoma, deletions on chromosome 11q are known to result in an increase in the total number of chromosomal breaks. The DNA double-strand break repair pathways mediated by NHEJ are often upregulated in cancer. DLG2, a candidate tumor suppressor gene on chromosome 11q, has previously been implicated in DNA repair.

Methods

We evaluated an association between gene expression and neuroblastoma patient outcome, risk categorization, and 11q status using publicly available microarray data from independent neuroblastoma patient datasets. Functional studies were conducted using comet assay and H2AX phosphorylation in neuroblastoma cell lines and in the fruit fly with UVC-induced DNA breaks.

Results

We show that the NHEJ genes PARP1 and FEN1 are over expressed in neuroblastoma and restoration of DLG2 impairs their gene and protein expression. When exposed to UVC radiation, cells with DLG2 over expression show less DNA fragmentation and induce apoptosis in a p53 S46 dependent manner. We could also confirm that DLG2 over expression results in CHK1 phosphorylation consistent with previous reports of G2/M maintenance.

Conclusions

Taken together, we show that DLG2 over expression increases p53 mediated apoptosis in response to etoposide and UVC mediated genotoxicity and reduced DNA replication machinery.

Place, publisher, year, edition, pages
Elsevier, 2022
Keywords
DLG2, DNA, Damage, Neuroblastoma, Cancer
National Category
Cancer and Oncology Cell and Molecular Biology
Research subject
Translational Medicine TRIM; Bioinformatics
Identifiers
urn:nbn:se:his:diva-20940 (URN)10.1016/j.dnarep.2022.103302 (DOI)000782613400003 ()35217496 (PubMedID)2-s2.0-85124996325 (Scopus ID)
Funder
Swedish Childhood Cancer Foundation, PR2016–0060Royal Physiographic Society in Lund
Note

CC BY 4.0

Corresponding author: E-mail address: simon.keane@his.se (S. Keane).

We thank the Swedish Childhood Cancer Fund [PR2016–0060], Jane and Dan Olsson Foundation [2020–29], Assar Gabrielssons Foundation [FB20–13], Nilsson-Ehle Endowments, Kungliga Fysiografiska sällskapet i Lund and University of Skövde for financial support.

Available from: 2022-02-25 Created: 2022-02-25 Last updated: 2022-12-16Bibliographically approved
Keane, S., Herring, M., Rolny, P., Wettergren, Y. & Ejeskär, K. (2022). Inflammation suppresses DLG2 expression decreasing inflammasome formation. Journal of Cancer Research and Clinical Oncology, 149(9), 2295-2311
Open this publication in new window or tab >>Inflammation suppresses DLG2 expression decreasing inflammasome formation
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2022 (English)In: Journal of Cancer Research and Clinical Oncology, ISSN 0171-5216, E-ISSN 1432-1335, Vol. 149, no 9, p. 2295-2311Article in journal (Refereed) Published
Abstract [en]

Purpose

Loss of expression of DLG2 has been identified in a number of cancers to contribute to the disease by resulting in increased tumor cell proliferation and poor survival. In light of the previous evidence that DLG2 alters the cell cycle and affects proliferation, combined with indications that DLG2 is involved in NLRP3 inflammasome axis we speculated that DLG2 has an immune function. So far, there is no data that clearly elucidates this role, and this study was designed to investigate DLG2 in inflammatory colon disease and in colon cancer as well as its impact on inflammasome induction.

Methods

The DLG2 expression levels were established in publicly available inflammation, colon cancer and mouse model datasets. The overexpression and silencing of DLG2 in colon cancer cells were used to determine the effect of DLG2 expression on the activation of the inflammasome and subsequent cytokine release.

Results

The expression of DLG2 is repressed in inflammatory colon diseases IBD and Ulcerative colitis as well as colorectal cancer tissue compared to healthy individuals. We subsequently show that induction with inflammatory agents in cell and animal models results in a biphasic alteration of DLG2 with an initial increase followed by an ensuing decrease. DLG2 overexpression leads to a significant increase in expression of IL1B, IκBζ and BAX, components that result in inflammasome formation. DLG2 silencing in THP1 cells resulted in increased release of IL-6 into the microenvironment which once used to treat bystander COLO205 cells resulted in an increase in STAT3 phosphorylation and an increase proliferating cells and more cells in the G2/M phase. Restoration of DLG2 to the colon resulted in reduced AKT and S6 signaling.

Conclusion

DLG2 expression is altered in response to inflammation in the gut as well as colon cancer, resulting in altered ability to form inflammasomes.

Trial registration

NCT03072641.

Place, publisher, year, edition, pages
Springer Nature Switzerland AG, 2022
Keywords
DLG2, Inflammasome, NFKBIZ, Ulcerative colitis, Colon cancer
National Category
Gastroenterology and Hepatology Immunology in the medical area
Research subject
Translational Medicine TRIM; Infection Biology
Identifiers
urn:nbn:se:his:diva-21117 (URN)10.1007/s00432-022-04029-7 (DOI)000789726400001 ()35499706 (PubMedID)2-s2.0-85129231846 (Scopus ID)
Funder
Royal Physiographic Society in Lund
Note

CC BY 4.0

Simon Keane simon.keane@his.se

Published: 02 May 2022

© 2022 Springer Nature Switzerland AG. Part of Springer Nature.

Springer

We thank the Jane and Dan Olsson foundation, Assar Gabrielssons Foundation, Royal Physiographic Society of Lund and University of Skövde for financial support. We thank the staff at the Centre for Cellular Imaging at the University of Gothenburg for their advice and assistance in fluorescence imaging. A-L. Helminen and H. Björkqvist are acknowledged for help with implementation of the NCT03072641 study and collection of patient samples. We thank L. Munro for clinical database assistance, and J. Flach and M. Åkerström for technical assistance.

Open access funding provided by University of Skövde. Jane and Dan Olsson foundation (2020–2029), Assar Gabrielssons Foundation (FB21-06), Royal Physiographic Society of Lund (NA) and University of Skövde.

The datasets generated during and/or analysed during the current study are available in the R2: genomics analysis visualization platform, http://r2.amc.n listed in the methods by GSE identification number.

Available from: 2022-05-04 Created: 2022-05-04 Last updated: 2022-08-15Bibliographically approved
Deland, L., Keane, S., Bontell, T. O., Fagman, H., Sjögren, H., Lind, A. E., . . . Abel, F. (2022). Novel TPR::ROS1 Fusion Gene Activates MAPK, PI3K and JAK/STAT Signaling in an Infant-type Pediatric Glioma. Cancer Genomics & Proteomics, 19(6), 711-726
Open this publication in new window or tab >>Novel TPR::ROS1 Fusion Gene Activates MAPK, PI3K and JAK/STAT Signaling in an Infant-type Pediatric Glioma
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2022 (English)In: Cancer Genomics & Proteomics, ISSN 1109-6535, E-ISSN 1790-6245, Vol. 19, no 6, p. 711-726Article in journal (Refereed) Published
Abstract [en]

BACKGROUND/AIM: Although fusion genes involving the proto-oncogene receptor tyrosine kinase ROS1 are rare in pediatric glioma, targeted therapies with small inhibitors are increasingly being approved for histology-agnostic fusion-positive solid tumors. PATIENT AND METHODS: Here, we present a 16-month-old boy, with a brain tumor in the third ventricle. The patient underwent complete resection but relapsed two years after diagnosis and underwent a second operation. The tumor was initially classified as a low-grade glioma (WHO grade 2); however, methylation profiling suggested the newly WHO-recognized type: infant-type hemispheric glioma. To further refine the molecular background, and search for druggable targets, whole genome (WGS) and whole transcriptome (RNA-Seq) sequencing was performed. RESULTS: Concomitant WGS and RNA-Seq analysis revealed several segmental gains and losses resulting in complex structural rearrangements and fusion genes. Among the top-candidates was a novel TPR::ROS1 fusion, for which only the 3' end of ROS1 was expressed in tumor tissue, indicating that wild type ROS1 is not normally expressed in the tissue of origin. Functional analysis by Western blot on protein lysates from transiently transfected HEK293 cells showed the TPR::ROS1 fusion gene to activate the MAPK-, PI3K- and JAK/STAT- pathways through increased phosphorylation of ERK, AKT, STAT and S6. The downstream pathway activation was also confirmed by immunohistochemistry on tumor tissue slides from the patient. CONCLUSION: We have mapped the activated oncogenic pathways of a novel ROS1-fusion gene and broadened the knowledge of the newly recognized infant-type glioma subtype. The finding facilitates suitable targeted therapies for the patient in case of relapse. 

Place, publisher, year, edition, pages
Cancer Genomics & Proteomics, 2022
Keywords
childhood cancer, chromosomal rearrangement, Pediatric glioma, precision medicine, TKI, tyrosine kinases
National Category
Cancer and Oncology Medical Genetics
Research subject
Translational Medicine TRIM
Identifiers
urn:nbn:se:his:diva-22033 (URN)10.21873/cgp.20354 (DOI)36316040 (PubMedID)2-s2.0-85140937065 (Scopus ID)
Funder
Swedish Cancer Society, 2018/825Swedish Cancer Society, 2018/652Swedish Childhood Cancer Foundation, PR2017-0029Swedish Childhood Cancer Foundation, PR2019-0079Swedish Childhood Cancer Foundation, KP2019-0010
Note

CC BY-NC-ND 4.0

Copyright © 2022, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Correspondence to: Frida Abel

This work was supported by the Swedish Cancer Society (www.cancerfonden.se, grant number 2018/825 to FA and grant number 2018/652 to JAN), the Swedish Children’s Cancer Foundation (www.barncancerfonden.se, grant number PR2017-0029 to FA, PR2019-0079 to KE, and KP2019-0010 to HC), and the ALF-agreement (www.researchweb.org/is/alfgbg, ALFGBG-716231 to FA, ALFGBG-965828 to HC, and ALFGBG-719301 to JAN).

Available from: 2022-11-10 Created: 2022-11-10 Last updated: 2023-01-16Bibliographically approved
Deland, L., Keane, S., Olsson Bontell, T., Sjögren, H., Fagman, H., Øra, I., . . . Abel, F. (2021). Discovery of a rare GKAP1-NTRK2 fusion in a pediatric low-grade glioma, leading to targeted treatment with TRK-inhibitor larotrectinib. Cancer Biology & Therapy, 22(3), 184-195
Open this publication in new window or tab >>Discovery of a rare GKAP1-NTRK2 fusion in a pediatric low-grade glioma, leading to targeted treatment with TRK-inhibitor larotrectinib
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2021 (English)In: Cancer Biology & Therapy, ISSN 1538-4047, E-ISSN 1555-8576, Vol. 22, no 3, p. 184-195Article in journal (Refereed) Published
Abstract [en]

Here we report a case of an 11-year-old girl with an inoperable tumor in the optic chiasm/hypothalamus, who experienced several tumor progressions despite three lines of chemotherapy treatment. Routine clinical examination classified the tumor as a BRAF-negative pilocytic astrocytoma. Copy-number variation profiling of fresh frozen tumor material identified two duplications in 9q21.32–33 leading to breakpoints within the GKAP1 and NTRK2 genes. RT-PCR Sanger sequencing revealed a GKAP1-NTRK2 exon 10–16 in-frame fusion, generating a putative fusion protein of 658 amino acids with a retained tyrosine kinase (TK) domain. Functional analysis by transient transfection of HEK293 cells showed the GKAP1-NTRK2 fusion protein to be activated through phosphorylation of the TK domain (Tyr705). Subsequently, downstream mediators of the MAPK- and PI3K-signaling pathways were upregulated in GKAP1-NTRK2 cells compared to NTRK2 wild-type; phosphorylated (p)ERK (3.6-fold), pAKT (1.8- fold), and pS6 ribosomal protein (1.4-fold). Following these findings, the patient was enrolled in a clinical trial and treated with the specific TRK-inhibitor larotrectinib, resulting in the arrest of tumor growth. The patient’s condition is currently stable and the quality of life has improved significantly. Our findings highlight the value of comprehensive clinical molecular screening of BRAF-negative pediatric low-grade gliomas, to reveal rare fusions serving as targets for precision therapy. 

Place, publisher, year, edition, pages
Taylor & Francis, 2021
Keywords
GKAP1, larotrectinib, NTRK2, pediatric brain tumor, pLGG, precision medicine, TRKB; fusion gene
National Category
Cancer and Oncology
Research subject
Translational Medicine TRIM
Identifiers
urn:nbn:se:his:diva-19649 (URN)10.1080/15384047.2021.1899573 (DOI)000636984900001 ()33820494 (PubMedID)2-s2.0-85103915136 (Scopus ID)
Funder
European Commission, PR2017-0029 PR2019-0079
Note

CC BY-NC-ND 4.0

© 2021 The Author(s). Published with license by Taylor & Francis Group, LLC.

Available from: 2021-04-22 Created: 2021-04-22 Last updated: 2022-10-26Bibliographically approved
Keane, S., Martinsson, T., Kogner, P. & Ejeskär, K. (2021). The loss of DLG2 isoform 7/8, but not isoform 2, is critical in advanced staged neuroblastoma. Cancer Cell International, 21(1), Article ID 170.
Open this publication in new window or tab >>The loss of DLG2 isoform 7/8, but not isoform 2, is critical in advanced staged neuroblastoma
2021 (English)In: Cancer Cell International, E-ISSN 1475-2867, Vol. 21, no 1, article id 170Article in journal (Refereed) Published
Abstract [en]

Background: Neuroblastoma is a childhood neural crest tumor showing large clinical and genetic heterogeneity, one form displaying 11q-deletion is very aggressive. It has been shown that 11q-deletion results in decreased expression of DLG2, a gene residing in the deleted region. DLG2 has a number of different isoforms with the main difference is the presence or absence of a L27 domain. The L27 domain containing DLG proteins can form complexes with CASK/MPP and LIN7 protein family members, which will control cell polarity and signaling. Methods: We evaluated the DLG gene family and the LIN7 gene family for their expression in differently INSS staged neuroblastoma from publically available data and primary tumors, we included two distinct DLG1 and DLG2 N-terminal transcript isoforms encoding L27 domains for their expression. Functionality of DLG2 isoforms and of LIN7A were evaluated in the 11q-deleted neuroblastoma cell line SKNAS. Results: In neuroblastoma only two DLG2 isoforms were expressed: isoform 2 and isoform 7/8. Using the array data we could determine that higher expression of DLG members that contain L27 domains correlated to better survival and prognosis. Whilst DLG1 showed a decrease in both isoforms with increased INSS stage, only the full length L27 containing DLG2 transcripts DLG2-isoform 7/8 showed a decrease in expression in high stage neuroblastoma. We could show that the protein encoded by DLG2-isoform 7 could bind to LIN7A, and increased DLG2-isoform 7 gene expression increased the expression of LIN7A, this reduced neuroblastoma cell proliferation and viability, with increased BAX/BCL2 ratio indicating increased apoptosis. Conclusion: We have provided evidence that gene expression of the L27 domain containing DLG2-isoform 7/8 but not L27 domain lacking DLG2-isoform 2 is disrupted in neuroblastoma, in particular in the aggressive subsets of tumors. The presence of the complete L27 domain allows for the binding to LIN7A, which will control cell polarity and signaling, thus affecting cancer cell viability. 

Place, publisher, year, edition, pages
Springer Nature, 2021
Keywords
DLG, DLG2, Isoform, L27, LIN7A, Neuroblastoma
National Category
Cancer and Oncology Cell and Molecular Biology
Research subject
Translational Medicine TRIM
Identifiers
urn:nbn:se:his:diva-19546 (URN)10.1186/s12935-021-01851-w (DOI)000629888200003 ()33726762 (PubMedID)2-s2.0-85102533029 (Scopus ID)
Note

CC BY 4.0

The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

© 2021, The Author(s).

© 2021 BioMed Central Ltd unless otherwise stated. Part of Springer Nature.

Correspondence: Katarina.ejeskar@his.se

Available from: 2021-03-25 Created: 2021-03-25 Last updated: 2023-09-08Bibliographically approved
Keane, S., Améen, S., Lindlöf, A. & Ejeskär, K. (2020). Low DLG2 gene expression, a link between 11q-deleted and MYCN-amplified neuroblastoma, causes forced cell cycle progression, and predicts poor patient survival. Cell Communication and Signaling, 18(1), Article ID 65.
Open this publication in new window or tab >>Low DLG2 gene expression, a link between 11q-deleted and MYCN-amplified neuroblastoma, causes forced cell cycle progression, and predicts poor patient survival
2020 (English)In: Cell Communication and Signaling, E-ISSN 1478-811X, Vol. 18, no 1, article id 65Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Neuroblastoma (NB) is a childhood neural crest tumor. There are two groups of aggressive NBs, one with MYCN amplification, and another with 11q chromosomal deletion; these chromosomal aberrations are generally mutually exclusive. The DLG2 gene resides in the 11q-deleted region, thus makes it an interesting NB candidate tumor suppressor gene. METHODS: We evaluated the association of DLG2 gene expression in NB with patient outcomes, stage and MYCN status, using online microarray data combining independent NB patient data sets. Functional studies were also conducted using NB cell models and the fruit fly. RESULTS: Using the array data we concluded that higher DLG2 expression was positively correlated to patient survival. We could also see that expression of DLG2 was inversely correlated with MYCN status and tumor stage. Cell proliferation was lowered in both 11q-normal and 11q-deleted NB cells after DLG2 over expression, and increased in 11q-normal NB cells after DLG2 silencing. Higher level of DLG2 increased the percentage of cells in the G2/M phase and decreased the percentage of cells in the G1 phase. We detected increased protein levels of Cyclin A and Cyclin B in fruit fly models either over expressing dMyc or with RNAi-silenced dmDLG, indicating that both events resulted in enhanced cell cycling. Induced MYCN expression in NB cells lowered DLG2 gene expression, which was confirmed in the fly; when dMyc was over expressed, the dmDLG protein level was lowered, indicating a link between Myc over expression and low dmDLG level. CONCLUSION: We conclude that low DLG2 expression level forces cell cycle progression, and that it predicts poor NB patient survival. The low DLG2 expression level could be caused by either MYCN-amplification or 11q-deletion. Video Abstract.

Place, publisher, year, edition, pages
BioMed Central (BMC), 2020
Keywords
11q, DLG2, MAGUK, MYCN, Neuroblastoma
National Category
Medical Genetics Cancer and Oncology
Research subject
Translational Medicine TRIM; Bioinformatics
Identifiers
urn:nbn:se:his:diva-18430 (URN)10.1186/s12964-020-00553-6 (DOI)000615918700002 ()32312269 (PubMedID)2-s2.0-85083811841 (Scopus ID)
Note

CC BY 4.0

Available from: 2020-05-07 Created: 2020-05-07 Last updated: 2023-10-23Bibliographically approved
Trindade, F., Saraiva, F., Keane, S., Leite-Moreira, A., Vitorino, R., Tajsharghi, H. & Falcão-Pires, I. (2020). Preoperative myocardial expression of E3 ubiquitin ligases in aortic stenosis patients undergoing valve replacement and their association to postoperative hypertrophy. PLOS ONE, 15(9), Article ID e0237000.
Open this publication in new window or tab >>Preoperative myocardial expression of E3 ubiquitin ligases in aortic stenosis patients undergoing valve replacement and their association to postoperative hypertrophy
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2020 (English)In: PLOS ONE, E-ISSN 1932-6203, Vol. 15, no 9, article id e0237000Article in journal (Refereed) Published
Abstract [en]

Currently, aortic valve replacement is the only treatment capable of relieving left ventricle pressure overload in patients with severe aortic stenosis. It aims to improve cardiac function and revert hypertrophy, by triggering myocardial reverse remodeling. Despite immediately relieving afterload, reverse remodeling turns out to be extremely variable. Among other factors, the extent of reverse remodeling may depend on how well ubiquitin-proteasome system tackle hypertrophy. Therefore, we assessed tagged ubiquitin and ubiquitin ligases in the left ventricle collected from patients undergoing valve replacement and tested their association to the degree of reverse remodeling. Patients were classified according to the regression of left ventricle mass (ΔLVM) and assigned to complete (ΔLVM≥15%) or incomplete (ΔLVM≤5%) reverse remodeling groups. No direct inter-group differences were observed. Nevertheless, correlation analysis supports a fundamental role of the ubiquitin-proteasome system during reverse remodeling. Indeed, total protein ubiquitination was associated to hypertrophic indexes such as interventricular septal thickness (r = 0.55, p = 0.03) and posterior wall thickness (r = 0.65, p = 0.009). No significant correlations were observed for Muscle Ring Finger 3. Surprisingly, though, higher levels of atrogin-1 were associated to postoperative interventricular septal thickness (r = 0.71, p = 0.005). In turn, Muscle Ring Finger 1 correlated negatively with this postoperative hypertrophy marker (r = -0.68, p = 0.005), suggesting a cardioprotective role during reverse remodeling. No significant correlations were found with left ventricle mass regression, although a trend for a negative association between the ligase Murine Double Minute 2 and mass regression (r = -0.44, p = 0.10) was found. Animal studies will be necessary to understand whether this ligase is protective or detrimental. Herein, we show, for the first time, an association between the preoperative myocardial levels of ubiquitin ligases and postoperative hypertrophy, highlighting the therapeutic potential of targeting ubiquitin ligases in incomplete reverse remodeling.

Place, publisher, year, edition, pages
PLOS, 2020
National Category
Cardiac and Cardiovascular Systems Other Medical Sciences
Research subject
Translational Medicine TRIM
Identifiers
urn:nbn:se:his:diva-19144 (URN)10.1371/journal.pone.0237000 (DOI)000573851100068 ()32946439 (PubMedID)2-s2.0-85091324224 (Scopus ID)
Note

CC BY 4.0

Available from: 2020-10-01 Created: 2020-10-01 Last updated: 2021-06-14Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-0471-6896

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