{"entity": "researcher", "timestamp": "2026-08-22T06:57:49.070Z", "family": "Agarwal", "given": "Prasoon", "initials": "P", "orcid": "0000-0003-1813-7606", "affiliations": ["Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba' Winnipeg' Canada (M.M.T., K.G.C., B.X., P.A., S.M.K., V.W.D.).", "Department of Pharmacology and Therapeutics (M.M.T., K.G.C., B.X., P.A., S.M.K., V.W.D.), University of Manitoba, Winnipeg, Canada.", "Rady Faculty of Health Science, College of Medicine (M.M.T., K.G.C., B.X., P.A., S.M.K., V.S., V.W.D.), University of Manitoba, Winnipeg, Canada.", "KTH Royal Institute of Technology, School of Electrical Engineering and Computer Science, Stockholm, Sweden (P.A.).", "Science for Life Laboratory, Solna, Sweden (P.A.)."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/84c99f839d45463aa14e7fbe322439ce.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/84c99f839d45463aa14e7fbe322439ce"}}, "publications": [{"entity": "publication", "iuid": "73262c787708424b9d25563ae3f8a88c", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/73262c787708424b9d25563ae3f8a88c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/73262c787708424b9d25563ae3f8a88c"}}, "title": "MYCN Amplification Is Associated with Reduced Expression of Genes Encoding \u03b3-Secretase Complex and NOTCH Signaling Components in Neuroblastoma.", "authors": [{"family": "Agarwal", "given": "Prasoon", "initials": "P", "orcid": "0000-0003-1813-7606", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/84c99f839d45463aa14e7fbe322439ce.json"}}, {"family": "Glowacka", "given": "Aleksandra", "initials": "A"}, {"family": "Mahmoud", "given": "Loay", "initials": "L"}, {"family": "Bazzar", "given": "Wesam", "initials": "W"}, {"family": "Larsson", "given": "Lars-Gunnar", "initials": "LG"}, {"family": "Alzrigat", "given": "Mohammad", "initials": "M", "orcid": "0000-0001-5514-8625", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/602febc530284c0790edbd2d1f4aa734.json"}}], "type": "journal article", "published": "2023-05-02", "journal": {"title": "Int J Mol Sci", "issn": "1422-0067", "volume": "24", "issue": "9", "issn-l": null}, "abstract": "Amplification of the MYCN oncogene is found in ~20% of neuroblastoma (NB) cases and correlates with high-risk disease and poor prognosis. Despite the plethora of studies describing the role of MYCN in NB, the exact molecular mechanisms underlying MYCN's contribution to high-risk disease are not completely understood. Herein, we implemented an integrative approach combining publicly available RNA-Seq and MYCN ChIP-Seq datasets derived from human NB cell lines to define biological processes directly regulated by MYCN in NB. Our approach revealed that MYCN-amplified NB cell lines, when compared to non-MYCN-amplified cell lines, are characterized by reduced expression of genes involved in NOTCH receptor processing, axoneme assembly, and membrane protein proteolysis. More specifically, we found genes encoding members of the \u03b3-secretase complex, which is known for its ability to liberate several intracellular signaling molecules from membrane-bound proteins such as NOTCH receptors, to be down-regulated in MYCN-amplified NB cell lines. Analysis of MYCN ChIP-Seq data revealed an enrichment of MYCN binding at the transcription start sites of genes encoding \u03b3-secretase complex subunits. Notably, using publicly available gene expression data from NB primary tumors, we revealed that the expression of \u03b3-secretase subunits encoding genes and other components of the NOTCH signaling pathway was also reduced in MYCN-amplified tumors and correlated with worse overall survival in NB patients. Genetic or pharmacological depletion of MYCN in NB cell lines induced the expression of \u03b3-secretase genes and NOTCH-target genes. Chemical inhibition of \u03b3-secretase activity dampened the expression of NOTCH-target genes upon MYCN depletion in NB cells. In conclusion, this study defines a set of MYCN-regulated pathways that are specific to MYCN-amplified NB tumors, and it suggests a novel role for MYCN in the suppression of genes of the \u03b3-secretase complex, with an impact on the NOTCH-target gene expression in MYCN-amplified NB.", "doi": "10.3390/ijms24098141", "pmid": "37175848", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC10179553"}, {"db": "pii", "key": "ijms24098141"}], "notes": [], "created": "2026-08-21T13:03:46.215Z", "modified": "2026-08-21T13:03:46.256Z"}, {"entity": "publication", "iuid": "a4da366bb1884075ad1301a02942d0fd", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/a4da366bb1884075ad1301a02942d0fd.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/a4da366bb1884075ad1301a02942d0fd"}}, "title": "Survivin Inhibition by Piperine Sensitizes Glioblastoma Cancer Stem Cells and Leads to Better Drug Response.", "authors": [{"family": "Warrier", "given": "Neerada Meenakshi", "initials": "NM", "orcid": "0000-0001-9321-2923", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9168f58729714ba78078ebd3cfdb1887.json"}}, {"family": "Krishnan", "given": "Ramesh Kumar", "initials": "RK"}, {"family": "Prabhu", "given": "Vijendra", "initials": "V", "orcid": "0000-0001-5927-2180", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2d42a40b917e49f2a2d5ab19e228f84f.json"}}, {"family": "Hariharapura", "given": "Raghu Chandrashekhar", "initials": "RC", "orcid": "0000-0002-6538-7758", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/770c56add28c4d3797db5252bafa4b85.json"}}, {"family": "Agarwal", "given": "Prasoon", "initials": "P", "orcid": "0000-0003-1813-7606", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/84c99f839d45463aa14e7fbe322439ce.json"}}, {"family": "Kumar", "given": "Praveen", "initials": "P", "orcid": "0000-0002-6330-7355", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/26c2bf9b534746ffb8b213b86ef6d3d6.json"}}], "type": "journal article", "published": "2022-07-09", "journal": {"title": "Int J Mol Sci", "issn": "1422-0067", "volume": "23", "issue": "14", "issn-l": null}, "abstract": "Glioblastoma multiforme (GBM) cancer stem cells (GSCs) are one of the strongest contributing factors to treatment resistance in GBM. Identification of biomarkers capable of directly affecting these cells within the bulk tumor is a major challenge associated with the development of new targeting strategies. In this study, we focus on understanding the potential of the multifunctional extraordinaire survivin as a biomarker for GSCs. We analyzed the expression profiles of this gene using various publicly available datasets to understand its importance in stemness and other cancer processes. The findings from these studies were further validated using human GSCs isolated from a GBM cell line. In these GSCs, survivin was inhibited using the dietary phytochemical piperine (PIP) and the subsequent effects on stemness, cancer processes and Temozolomide were investigated. In silico analysis identified survivin to be one of the most significant differentially regulated gene in GSCs, in comparison to common stemness markers. Further validation studies on the isolated GSCs showed the importance of survivin in stemness, cancer progression and therapy resistance. Taken together, our study identifies survivin as a more consistent GSC marker and also suggests the possibility of using survivin inhibitors along with standard of care drugs for better therapeutic outcomes.", "doi": "10.3390/ijms23147604", "pmid": "35886952", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9323232"}, {"db": "pii", "key": "ijms23147604"}], "notes": [], "created": "2026-08-21T13:03:31.527Z", "modified": "2026-08-21T13:03:31.656Z"}, {"entity": "publication", "iuid": "7f74c23da3ee4df08069d96e0acc2c23", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/7f74c23da3ee4df08069d96e0acc2c23.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/7f74c23da3ee4df08069d96e0acc2c23"}}, "title": "Mitochondrial Sirtuin-3 (SIRT3) Prevents Doxorubicin-Induced Dilated Cardiomyopathy by Modulating Protein Acetylation and Oxidative Stress.", "authors": [{"family": "Tomczyk", "given": "Mateusz M", "initials": "MM", "orcid": "0000-0001-6557-2737", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/da0fdabe5fd84fa5b605c75a6972ec6a.json"}}, {"family": "Cheung", "given": "Kyle G", "initials": "KG", "orcid": "0000-0002-5219-0956", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3c1f743d456f49ab889d986600a60768.json"}}, {"family": "Xiang", "given": "Bo", "initials": "B", "orcid": "0000-0002-0919-6121", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6594905bc6af4dfbb4bd6729540780ff.json"}}, {"family": "Tamanna", "given": "Nahid", "initials": "N", "orcid": "0000-0001-7134-7173", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/797faa6031794d899f9fc8c8fddf66a1.json"}}, {"family": "Fonseca Teixeira", "given": "Ana L", "initials": "AL", "orcid": "0000-0002-9639-3413", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3d734ea3740b4f318a8dcfa06d969d3f.json"}}, {"family": "Agarwal", "given": "Prasoon", "initials": "P", "orcid": "0000-0003-1813-7606", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/84c99f839d45463aa14e7fbe322439ce.json"}}, {"family": "Kereliuk", "given": "Stephanie M", "initials": "SM", "orcid": "0000-0003-0293-5646", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ebbdb4d8c46a47cabf5b51ec06d9f533.json"}}, {"family": "Spicer", "given": "Victor", "initials": "V", "orcid": "0000-0002-9097-1913", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e6ba024f1f454600936824634323d07b.json"}}, {"family": "Lin", "given": "Ligen", "initials": "L", "orcid": "0000-0002-6799-5327", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/da00574f43dd443296095a2dae78411a.json"}}, {"family": "Treberg", "given": "Jason", "initials": "J", "orcid": "0000-0001-5112-7325", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b40c6b84d17f42a7bd832ca169bb3bb7.json"}}, {"family": "Tong", "given": "Qiang", "initials": "Q", "orcid": "0000-0003-1016-1839", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/937ecd4328404807a00fe0aaa392b181.json"}}, {"family": "Dolinsky", "given": "Vernon W", "initials": "VW", "orcid": "0000-0001-5191-4628", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/325bbaf75a364eb6afd3c3e5db560d84.json"}}], "type": "journal article", "published": "2022-05-00", "journal": {"title": "Circ Heart Fail", "issn": "1941-3297", "volume": "15", "issue": "5", "pages": "e008547", "issn-l": "1941-3289"}, "abstract": "High doses of doxorubicin put cancer patients at risk for developing dilated cardiomyopathy. Previously, we showed that doxorubicin treatment decreases SIRT3 (sirtuin 3), the main mitochondrial deacetylase and increases protein acetylation in rat cardiomyocytes. Here, we hypothesize that SIRT3 expression can attenuate doxorubicin induced dilated cardiomyopathy in vivo by preventing the acetylation of mitochondrial proteins.\n\nNontransgenic, M3-SIRT3 (truncated SIRT3; short isoform), and M1-SIRT3 (full-length SIRT3; mitochondrial localized) transgenic mice were treated with doxorubicin for 4 weeks (8 mg/kg body weight per week). Echocardiography was performed to assess cardiac structure and function and validated by immunohistochemistry and immunofluorescence (n=4-10). Mass spectrometry was performed on cardiac mitochondrial peptides in saline (n=6) and doxorubicin (n=5) treated hearts. Validation was performed in doxorubicin treated primary rat and human induced stem cell derived cardiomyocytes transduced with adenoviruses for M3-SIRT3 and M1-SIRT3 and deacetylase deficient mutants (n=4-10).\n\nEchocardiography revealed that M3-SIRT3 transgenic mice were partially resistant to doxorubicin induced changes to cardiac structure and function whereas M1-SIRT3 expression prevented cardiac remodeling and dysfunction. In doxorubicin hearts, 37 unique acetylation sites on mitochondrial proteins were altered. Pathway analysis revealed these proteins are involved in energy production, fatty acid metabolism, and oxidative stress resistance. Increased M1-SIRT3 expression in primary rat and human cardiomyocytes attenuated doxorubicin-induced superoxide formation, whereas deacetylase deficient mutants were unable to prevent oxidative stress.\n\nDoxorubicin reduced SIRT3 expression and markedly affected the cardiac mitochondrial acetylome. Increased M1-SIRT3 expression in vivo prevented doxorubicin-induced cardiac dysfunction, suggesting that SIRT3 could be a potential therapeutic target for mitigating doxorubicin-induced dilated cardiomyopathy.", "doi": "10.1161/CIRCHEARTFAILURE.121.008547", "pmid": "35418250", "labels": [], "xrefs": [{"db": "mid", "key": "NIHMS1786476"}, {"db": "pmc", "key": "PMC9117478"}], "notes": [], "created": "2026-08-21T12:31:02.601Z", "modified": "2026-08-21T12:31:03.200Z"}, {"entity": "publication", "iuid": "aecbf4d086604e75b03d2c2b9eeda7ca", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/aecbf4d086604e75b03d2c2b9eeda7ca.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/aecbf4d086604e75b03d2c2b9eeda7ca"}}, "title": "Integrative Analysis to Identify Genes Associated with Stemness and Immune Infiltration in Glioblastoma.", "authors": [{"family": "Warrier", "given": "Neerada Meenakshi", "initials": "NM", "orcid": "0000-0001-9321-2923", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9168f58729714ba78078ebd3cfdb1887.json"}}, {"family": "Agarwal", "given": "Prasoon", "initials": "P", "orcid": "0000-0003-1813-7606", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/84c99f839d45463aa14e7fbe322439ce.json"}}, {"family": "Kumar", "given": "Praveen", "initials": "P", "orcid": "0000-0002-6330-7355", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/26c2bf9b534746ffb8b213b86ef6d3d6.json"}}], "type": "journal article", "published": "2021-10-15", "journal": {"title": "Cells", "issn": "2073-4409", "volume": "10", "issue": "10", "issn-l": "2073-4409"}, "abstract": "It is imperative to identify the mechanisms that confer stemness to the cancer cells for more effective targeting. Moreover, there are not many studies on the link between stemness characteristics and the immune response in tumours. Therefore, in the current study involving GBM, we started with the study of BIRC5 (one of the rare genes differentially expressed in normal and cancer cells) and CXCR4 (gene involved in the survival and proliferation of CSCs). Together, these genes have not been systematically explored. We used a set of 27 promoter methylated regions in GBM. Our analysis showed that four genes corresponding to these regions, namely EOMES, BDNF, HLA-A, and PECAM1, were involved with BIRC5 and CXCR4. Interestingly, we found EOMES to be very significantly involved in stemness and immunology and it was positively correlated to CXCR4. Additionally, BDNF, which was significant in methylation, was negatively correlated to BIRC5.", "doi": "10.3390/cells10102765", "pmid": "34685742", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8534801"}, {"db": "pii", "key": "cells10102765"}], "notes": [], "created": "2026-08-21T13:02:03.592Z", "modified": "2026-08-21T13:02:03.728Z"}, {"entity": "publication", "iuid": "a6044d8b7a8944b390b0f47c62ede2d4", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/a6044d8b7a8944b390b0f47c62ede2d4.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/a6044d8b7a8944b390b0f47c62ede2d4"}}, "title": "Integration of the Microbiome, Metabolome and Transcriptomics Data Identified Novel Metabolic Pathway Regulation in Colorectal Cancer.", "authors": [{"family": "Bisht", "given": "Vartika", "initials": "V"}, {"family": "Nash", "given": "Katrina", "initials": "K", "orcid": "0000-0002-5204-9688", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e74cbe386dca42f08edbbb2b40f8688a.json"}}, {"family": "Xu", "given": "Yuanwei", "initials": "Y", "orcid": "0000-0002-2337-3999", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6dc173aba08d40169a2a24f7bec00aad.json"}}, {"family": "Agarwal", "given": "Prasoon", "initials": "P", "orcid": "0000-0003-1813-7606", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/84c99f839d45463aa14e7fbe322439ce.json"}}, {"family": "Bosch", "given": "Sofie", "initials": "S"}, {"family": "Gkoutos", "given": "Georgios V", "initials": "GV", "orcid": "0000-0002-2061-091X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1047ac3de3334d649701f565a78cfc1f.json"}}, {"family": "Acharjee", "given": "Animesh", "initials": "A", "orcid": "0000-0003-2735-7010", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a22e43fa951b4c0fac3608e2db12cc30.json"}}], "type": "journal article", "published": "2021-05-28", "journal": {"title": "Int J Mol Sci", "issn": "1422-0067", "volume": "22", "issue": "11", "issn-l": null}, "abstract": "Integrative multiomics data analysis provides a unique opportunity for the mechanistic understanding of colorectal cancer (CRC) in addition to the identification of potential novel therapeutic targets. In this study, we used public omics data sets to investigate potential associations between microbiome, metabolome, bulk transcriptomics and single cell RNA sequencing datasets. We identified multiple potential interactions, for example 5-aminovalerate interacting with Adlercreutzia; cholesteryl ester interacting with bacterial genera Staphylococcus, Blautia and Roseburia. Using public single cell and bulk RNA sequencing, we identified 17 overlapping genes involved in epithelial cell pathways, with particular significance of the oxidative phosphorylation pathway and the ACAT1 gene that indirectly regulates the esterification of cholesterol. These findings demonstrate that the integration of multiomics data sets from diverse populations can help us in untangling the colorectal cancer pathogenesis as well as postulate the disease pathology mechanisms and therapeutic targets.", "doi": "10.3390/ijms22115763", "pmid": "34071236", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8198673"}, {"db": "pii", "key": "ijms22115763"}], "notes": [], "created": "2026-08-21T13:03:20.822Z", "modified": "2026-08-21T13:03:21.049Z"}]}