Bioinformatics analysis of miRNAs in the neuroblastoma 11q-deleted region reveals a role of miR-548l in both 11q-deleted and MYCN amplified tumour cellsShow others and affiliations
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. Vol. 12, no 1, article id 19729
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: urn:nbn:se:his:diva-22068DOI: 10.1038/s41598-022-24140-6ISI: 000885172100065PubMedID: 36396668Scopus ID: 2-s2.0-85142197814OAI: oai:DiVA.org:his-22068DiVA, id: diva2:1712309
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.
2022-11-212022-11-212023-01-16Bibliographically approved