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miR‐186 Inhibition Alters Cell Proliferation and Colony Formation in Prostate Cancer
Author(s) -
Jones Dominique,
Hobbing Katharine,
Schmidt M.,
Clark Geoffrey,
Kidd LaCreis
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.284.4
Subject(s) - microrna , viability assay , cell growth , cancer research , biology , transfection , prostate cancer , metastasis , cell , biomarker , cell culture , cancer , gene , genetics
Numerous published reports show microRNAs (miRs) influence PCA development and disease progression. However, there are no published reports on the role of miR‐186 in relation to PCA. Previously, we observed miR‐186 expression was significantly up‐regulated in the serum of PCA patients (n = 15) diagnosed with stage III and IV disease compared to controls (n = 5). We also observed miR‐186 expression was significantly up‐regulated in metastatic PCA cells (PC3) after normalization with control cell line (RWPE1) and endogenous miR (U6). Mir‐186 overexpression is associated with the down‐regulation of pro‐apoptotic and tumor suppression‐related genes in various cancers. We hypothesized that miR‐186 inhibition will reduce the aggressive PCA phenotype. To test this hypothesis, PC3 cells were transiently transfected with miR‐186 inhibitor and scramble control for 24hrs. Cell viability and colony formation of transfected cells were evaluated via ATPlite and soft agar assays, respectively. MiR‐186 inhibition significantly decreased both cell viability by 48‐58% at 72‐96hrs and colony formation by 30% after 21 days. These findings suggest miR‐186 inhibition represses cell proliferation and anchorage independence. Additional studies are needed to: (1) discern whether stable miR‐186 inhibition will reduce cell migration, invasion and metastasis using in vitro assays and murine models; (2) identify and validate miR‐186 targets using gene/protein analyses. Such efforts will lead to the identification of a biomarker to help improve current PCA detection, prognostic and clinical management strategies.