BACKGROUND: MicroRNAs (miRNAs) are small, non-coding RNAs (18-25 nucleotides) that post-transcriptionally modulate gene expression by negatively regulating the stability or translational efficiency of their target mRNAs. The aim of this study was to investigate the expression pattern of microRNA-107 (miR-107) in human breast cancer, and its potential role in disease pathogenesis. METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to determine the expression level of miR-107 in 30 breast cancer specimens and adjacent normal breast tissues. MTT and colony formation assays, transwell and wound healing test, cell cycle assays were conducted to explore the potential function of miR-107 in human MDA-MB-231 breast cancer cells. Luciferase reporter assays were employed to validate regulation of a putative target of miR-107. The effect of modulating miR-107 on endogenous levels of this target were subsequently confirmed via Western blotting. RESULTS: miR-107 expression was relatively decreased in breast cancer specimens compared with adjacent normal tissues (P<0.01). Overexpression of miR-107 suppressed MDA-MB-231 cell proliferation and migration, meanwhile the cells were arrested at G0/G1 phase. Luciferase assays using a reporter carrying a putative miR-107 target site in the 3', untranslated region (3'-UTR) of CDK8 revealed that miR-107 directly targets CDK8. Overexpression of miR-107 led to downregulation of CDK8 at the mRNA and protein level, as assessed by Western blotting. CONCLUSIONS: miR-107 may play an important role in breast cancer progression, which might negatively regulate the expression of CDK8 and inhibit the proliferation and migration of MDA-MB-231 cell line.
BACKGROUND: MicroRNAs (miRNAs) are small, non-coding RNAs (18-25 nucleotides) that post-transcriptionally modulate gene expression by negatively regulating the stability or translational efficiency of their target mRNAs. The aim of this study was to investigate the expression pattern of microRNA-107 (miR-107) in humanbreast cancer, and its potential role in disease pathogenesis. METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to determine the expression level of miR-107 in 30 breast cancer specimens and adjacent normal breast tissues. MTT and colony formation assays, transwell and wound healing test, cell cycle assays were conducted to explore the potential function of miR-107 in human MDA-MB-231 breast cancer cells. Luciferase reporter assays were employed to validate regulation of a putative target of miR-107. The effect of modulating miR-107 on endogenous levels of this target were subsequently confirmed via Western blotting. RESULTS:miR-107 expression was relatively decreased in breast cancer specimens compared with adjacent normal tissues (P<0.01). Overexpression of miR-107 suppressed MDA-MB-231 cell proliferation and migration, meanwhile the cells were arrested at G0/G1 phase. Luciferase assays using a reporter carrying a putative miR-107 target site in the 3', untranslated region (3'-UTR) of CDK8 revealed that miR-107 directly targets CDK8. Overexpression of miR-107 led to downregulation of CDK8 at the mRNA and protein level, as assessed by Western blotting. CONCLUSIONS:miR-107 may play an important role in breast cancer progression, which might negatively regulate the expression of CDK8 and inhibit the proliferation and migration of MDA-MB-231 cell line.
Authors: Remco Nagel; Carlos le Sage; Begoña Diosdado; Maike van der Waal; Joachim A F Oude Vrielink; Anne Bolijn; Gerrit A Meijer; Reuven Agami Journal: Cancer Res Date: 2008-07-15 Impact factor: 12.701
Authors: Adam S Adler; Mark L McCleland; Tom Truong; Shari Lau; Zora Modrusan; Tim M Soukup; Merone Roose-Girma; Elizabeth M Blackwood; Ron Firestein Journal: Cancer Res Date: 2012-02-16 Impact factor: 12.701
Authors: D Tryfonopoulos; S Walsh; D M Collins; L Flanagan; C Quinn; B Corkery; E W McDermott; D Evoy; A Pierce; N O'Donovan; J Crown; M J Duffy Journal: Ann Oncol Date: 2011-02-28 Impact factor: 32.976
Authors: Jilong Li; Subhadip Ghatak; Mohamed S El Masry; Amitava Das; Yang Liu; Sashwati Roy; Robert J Lee; Chandan K Sen Journal: Mol Ther Date: 2018-04-27 Impact factor: 11.454