{"entity": "researcher", "timestamp": "2026-08-17T02:24:51.593Z", "family": "Kanduri", "given": "Chandrasekhar", "initials": "C", "orcid": "0000-0001-6271-9078", "affiliations": ["Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden. kanduri.chandrasekhar@gu.se."], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/a8da9c5c5d0c48f9ae08549027375512.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/a8da9c5c5d0c48f9ae08549027375512"}}, "publications": [{"entity": "publication", "iuid": "dd3b9e495f154236a9c26473858d9e33", "links": {"self": {"href": "https://publications.scilifelab.se/publication/dd3b9e495f154236a9c26473858d9e33.json"}, "display": {"href": "https://publications.scilifelab.se/publication/dd3b9e495f154236a9c26473858d9e33"}}, "title": "IER3: exploring its dual function as an oncogene and tumor suppressor.", "authors": [{"family": "Kanduri", "given": "Meena", "initials": "M", "orcid": "0000-0003-2781-4779", "researcher": {"href": "https://publications.scilifelab.se/researcher/b0c8993f8119475d98d8f4ca1e77abff.json"}}, {"family": "Subhash", "given": "Santhilal", "initials": "S", "orcid": "0000-0002-0077-4597", "researcher": {"href": "https://publications.scilifelab.se/researcher/4ca22115b7c9444ab2056126a1c9d36d.json"}}, {"family": "Putino", "given": "Rossana", "initials": "R"}, {"family": "Mahale", "given": "Sagar", "initials": "S"}, {"family": "Kanduri", "given": "Chandrasekhar", "initials": "C", "orcid": "0000-0001-6271-9078", "researcher": {"href": "https://publications.scilifelab.se/researcher/a8da9c5c5d0c48f9ae08549027375512.json"}}], "type": "journal article", "published": "2025-04-00", "journal": {"title": "Cancer Gene Ther", "issn": "1476-5500", "volume": "32", "issue": "4", "pages": "450-463", "issn-l": null}, "abstract": "The IER3 gene has a complex role in cancer biology, acting either as a tumor suppressor or an oncogene, depending on the cancer type. This duality underscores the complexity and importance of molecular pathways in modulating cancer behavior. Despite its significance in cancer development, there is a dearth of studies elucidating the exact mechanisms underlying IER3's involvement in modulating cancer behavior. Here, utilizing cervical carcinoma and neuroblastoma (NB) cell lines as model systems we characterized the pathways that mediate the functional switch between the oncogenic and tumor suppressor roles of IER3. In HeLa cells, IER3 expression promotes an oncogenic program that includes immediate early response pathway genes such as EGR2, FOS, and JUN. However, in NB cells, IER3 suppresses the EGR2-dependent oncogenic program. This differential regulation of EGR2 by IER3 involves epigenetic modulation of the EGR2 promoter. IER3 dependent tumor suppressor pathway in NB cells relies on ADAM19 gene. Thus, our findings uncover the molecular pathways that dictate the context-dependent roles of IER3 in cancer, providing insights into its dual functionality in different cancer types.", "doi": "10.1038/s41417-025-00891-y", "pmid": "40090972", "labels": {"Bioinformatics Support for Computational Resources": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC11976266"}, {"db": "pii", "key": "10.1038/s41417-025-00891-y"}], "notes": [], "created": "2025-11-28T10:44:57.184Z", "modified": "2025-11-28T10:44:57.463Z"}, {"entity": "publication", "iuid": "f2d9ecae73c44d238c01ab6c6878d296", "links": {"self": {"href": "https://publications.scilifelab.se/publication/f2d9ecae73c44d238c01ab6c6878d296.json"}, "display": {"href": "https://publications.scilifelab.se/publication/f2d9ecae73c44d238c01ab6c6878d296"}}, "title": "LY6K-AS lncRNA is a lung adenocarcinoma prognostic biomarker and regulator of mitotic progression.", "authors": [{"family": "Ali", "given": "Mohamad Moustafa", "initials": "MM"}, {"family": "Di Marco", "given": "Mirco", "initials": "M", "orcid": "0000-0001-8890-233X", "researcher": {"href": "https://publications.scilifelab.se/researcher/8406c87db9604c1e863736eb7bd11bf1.json"}}, {"family": "Mahale", "given": "Sagar", "initials": "S"}, {"family": "Jachimowicz", "given": "Daniel", "initials": "D"}, {"family": "Kosalai", "given": "Subazini Thankaswamy", "initials": "ST"}, {"family": "Reischl", "given": "Silke", "initials": "S", "orcid": "0000-0003-4822-4137", "researcher": {"href": "https://publications.scilifelab.se/researcher/bf139e277ad14d7caf0bfe88ef9f34d2.json"}}, {"family": "Statello", "given": "Luisa", "initials": "L"}, {"family": "Mishra", "given": "Kankadeb", "initials": "K"}, {"family": "Darnfors", "given": "Catarina", "initials": "C"}, {"family": "Kanduri", "given": "Meena", "initials": "M"}, {"family": "Kanduri", "given": "Chandrasekhar", "initials": "C", "orcid": "0000-0001-6271-9078", "researcher": {"href": "https://publications.scilifelab.se/researcher/a8da9c5c5d0c48f9ae08549027375512.json"}}], "type": "journal article", "published": "2021-04-00", "journal": {"title": "Oncogene", "issn": "1476-5594", "volume": "40", "issue": "13", "pages": "2463-2478", "issn-l": "0950-9232"}, "abstract": "Recent advances in genomics unraveled several actionable mutational drivers in lung cancer, leading to promising therapies such as tyrosine kinase inhibitors and immune checkpoint inhibitors. However, the tumors' acquired resistance to the newly-developed as well as existing therapies restricts life quality improvements. Therefore, we investigated the noncoding portion of the human transcriptome in search of alternative actionable targets. We identified an antisense transcript, LY6K-AS, with elevated expression in lung adenocarcinoma (LUAD) patients, and its higher expression in LUAD patients predicts poor survival outcomes. LY6K-AS abrogation interfered with the mitotic progression of lung cancer cells resulting in unfaithful chromosomal segregation. LY6K-AS interacts with and stabilizes 14-3-3 proteins to regulate the transcription of kinetochore and mitotic checkpoint proteins. We also show that LY6K-AS regulates the levels of histone H3 lysine 4 trimethylation (H3K4me3) at the promoters of kinetochore members. Cisplatin treatment and LY6K-AS silencing affect many common pathways enriched in cell cycle-related functions. LY6K-AS silencing affects the growth of xenografts derived from wildtype and cisplatin-resistant lung cancer cells. Collectively, these data indicate that LY6K-AS silencing is a promising therapeutic option for LUAD that inhibits oncogenic mitotic progression.", "doi": "10.1038/s41388-021-01696-7", "pmid": "33674747", "labels": {"Integrated Microscopy Technologies Gothenburg": "Service"}, "xrefs": [{"db": "pii", "key": "10.1038/s41388-021-01696-7"}], "notes": [], "created": "2023-02-16T08:13:43.139Z", "modified": "2023-02-16T08:13:43.241Z"}]}