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dc.contributor.authorMatin, Farhana
dc.contributor.authorJeet, Varinder
dc.contributor.authorSrinivasan, Srilakshmi
dc.contributor.authorCristino, Alexandre S
dc.contributor.authorPanchadsaram, Janaththani
dc.contributor.authorClements, Judith A
dc.contributor.authorBatra, Jyotsna
dc.contributor.authorAustralian Prostate Cancer BioResource
dc.date.accessioned2020-06-25T00:16:47Z
dc.date.available2020-06-25T00:16:47Z
dc.date.issued2019
dc.identifier.issn1530-8561
dc.identifier.doi10.1373/clinchem.2018.295824
dc.identifier.urihttp://hdl.handle.net/10072/394865
dc.description.abstractBACKGROUND: MicroRNAs mediate biological processes through preferential binding to the 3′ untranslated region (3′ UTR) of target genes. Studies have shown their association with prostate cancer (PCa) risk through single-nucleotide polymorphisms (SNPs), known as miRSNPs. In a European cohort, 22 PCa risk-associated miRSNPs have been identified. The most significant miRSNP in the 3′ UTR of Kallikrein-related peptidase 3 (KLK3) created a binding site for miR-3162-5p. Here we investigated the miR-3162-5p–KLK interaction and the clinical implication of miR-3162-5p in PCa. METHODS: We tested the role of miR-3162-5p in PCa etiology using IncuCyte live-cell imaging and anchorage-independent growth assays. The effect of miR-3162-5p on KLK and androgen receptor (AR) expression was measured by RT-quantitative (q)PCR and target pulldown assays. KLK3 proteolytic activity was determined by DELFIA® immunoassay. Mass spectrometry identified pathways affected by miR-3162-5p. miR-3162-5p expression was measured in clinical samples using RT-qPCR. RESULTS: miR-3162-5p affected proliferation, migration, and colony formation of LNCaP cells by regulating the expression of KLK2–4 and AR by direct targeting. KLK3 protein expression was regulated by miR-3162-5p consistent with lower KLK3 proteolytic activity observed in LNCaP-conditioned media. KLK/AR pulldown and mass spectrometry analysis showed a potential role of miR-3162-5p in metabolic pathways via KLK/AR and additional targets. Increased miR-3162-5p expression was observed in prostate tumor tissues with higher Gleason grade. CONCLUSIONS: Our study provides an insight into possible involvement of miR-3162-5p in PCa etiology by targeting KLKs and AR. It highlights clinical utility of miR-3162-5p and its interactive axis as a new class of biomarkers and therapeutic targets for PCa.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherOxford University Press (OUP)
dc.relation.ispartofpagefrom771
dc.relation.ispartofpageto780
dc.relation.ispartofissue6
dc.relation.ispartofjournalClinical Chemistry
dc.relation.ispartofvolume65
dc.subject.fieldofresearchMedical Biotechnology
dc.subject.fieldofresearchMedical Biochemistry and Metabolomics
dc.subject.fieldofresearchClinical Sciences
dc.subject.fieldofresearchcode1004
dc.subject.fieldofresearchcode1101
dc.subject.fieldofresearchcode1103
dc.titleMicroRNA-3162-5p-Mediated Crosstalk between Kallikrein Family Members Including Prostate-Specific Antigen in Prostate Cancer
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationMatin, F; Jeet, V; Srinivasan, S; Cristino, AS; Panchadsaram, J; Clements, JA; Batra, J, MicroRNA-3162-5p-Mediated Crosstalk between Kallikrein Family Members Including Prostate-Specific Antigen in Prostate Cancer, Clinical Chemistry, 2019, 65 (6), pp. 771-780
dc.date.updated2020-06-25T00:14:59Z
gro.hasfulltextNo Full Text
gro.griffith.authorCristino, Alex


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