Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/30556
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dc.contributor.authorChi, Lap Hing-
dc.contributor.authorCross, Ryan S N-
dc.contributor.authorRedvers, Richard P-
dc.contributor.authorDavis, Melissa-
dc.contributor.authorHediyeh-Zadeh, Soroor-
dc.contributor.authorMathivanan, Suresh-
dc.contributor.authorSamuel, Monisha-
dc.contributor.authorLucas, Erin C-
dc.contributor.authorMouchemore, Kellie-
dc.contributor.authorGregory, Philip A-
dc.contributor.authorJohnstone, Cameron N-
dc.contributor.authorAnderson, Robin L-
dc.date2022-
dc.date.accessioned2022-07-19T06:57:59Z-
dc.date.available2022-07-19T06:57:59Z-
dc.date.issued2022-07-11-
dc.identifier.citationOncogenesis 2022; 11(1): 38en
dc.identifier.issn2157-9024
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/30556-
dc.description.abstractMiR-21 was identified as a gene whose expression correlated with the extent of metastasis of murine mammary tumours. Since miR-21 is recognised as being associated with poor prognosis in cancer, we investigated its contribution to mammary tumour growth and metastasis in tumours with capacity for spontaneous metastasis. Unexpectedly, we found that suppression of miR-21 activity in highly metastatic tumours resulted in regression of primary tumour growth in immunocompetent mice but did not impede growth in immunocompromised mice. Analysis of the immune infiltrate of the primary tumours at the time when the tumours started to regress revealed an influx of both CD4+ and CD8+ activated T cells and a reduction in PD-L1+ infiltrating monocytes, providing an explanation for the observed tumour regression. Loss of anti-tumour immune suppression caused by decreased miR-21 activity was confirmed by transcriptomic analysis of primary tumours. This analysis also revealed reduced expression of genes associated with cell cycle progression upon loss of miR-21 activity. A second activity of miR-21 was the promotion of metastasis as shown by the loss of metastatic capacity of miR-21 knockdown tumours established in immunocompromised mice, despite no impact on primary tumour growth. A proteomic analysis of tumour cells with altered miR-21 activity revealed deregulation of proteins known to be associated with tumour progression. The development of therapies targeting miR-21, possibly via targeted delivery to tumour cells, could be an effective therapy to combat primary tumour growth and suppress the development of metastatic disease.en
dc.language.isoeng
dc.titleMicroRNA-21 is immunosuppressive and pro-metastatic via separate mechanisms.en
dc.typeJournal Articleen
dc.identifier.journaltitleOncogenesisen
dc.identifier.affiliationOlivia Newton-John Cancer Research Instituteen
dc.identifier.affiliationImmunology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia..en
dc.identifier.affiliationFaculty of Health and Medical Sciences, The University of Adelaide, Adelaide, SA, Australia..en
dc.identifier.affiliationBioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia..en
dc.identifier.affiliationDepartment of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, VIC, Australia..en
dc.identifier.affiliationDivision of Immunology and Allergy, Department of Medicine, Karolinska Institute, Solna, Sweden..en
dc.identifier.affiliationSchool of Cancer Medicine, La Trobe University, Bundoora, VIC, Australia..en
dc.identifier.affiliationCentre for Cancer Biology, University of South Australia, Adelaide, SA, Australia..en
dc.identifier.affiliationDepartment of Clinical Pathology, University of Melbourne, Melbourne, VIC, Australia..en
dc.identifier.affiliationPeter MacCallum Cancer Centre, Parkville, VIC, Australia..en
dc.identifier.doi10.1038/s41389-022-00413-7en
dc.type.contentTexten
dc.identifier.orcidhttp://orcid.org/0000-0003-0983-3474en
dc.identifier.orcidhttp://orcid.org/0000-0002-7290-5795en
dc.identifier.orcidhttp://orcid.org/0000-0003-3577-7605en
dc.identifier.orcidhttp://orcid.org/0000-0002-6841-7422en
dc.identifier.orcidhttp://orcid.org/0000-0003-4527-7938en
dc.identifier.orcidhttp://orcid.org/0000-0001-6329-3785en
dc.identifier.orcidhttp://orcid.org/ 0000-0002-6464-8661en
dc.identifier.pubmedid35821197
local.name.researcherAnderson, Robin L
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
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