RGD Reference Report - miRNA-30a functions as a tumor suppressor by downregulating cyclin E2 expression in castration-resistant prostate cancer. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

miRNA-30a functions as a tumor suppressor by downregulating cyclin E2 expression in castration-resistant prostate cancer.

Authors: Zhang, Lei  Zhang, Xiao-Wen  Liu, Chun-Hui  Lu, Kai  Huang, Ye-Qing  Wang, Yi-Duo  Xing, Li  Zhang, Li-Jie  Liu, Ning  Jiang, Hua  Sun, Chao  Yang, Yu  Chen, Shu-Qiu  Chen, Ming  Xu, Bin 
Citation: Zhang L, etal., Mol Med Rep. 2016 Sep;14(3):2077-84. doi: 10.3892/mmr.2016.5469. Epub 2016 Jul 6.
RGD ID: 13504681
Pubmed: PMID:27431942   (View Abstract at PubMed)
DOI: DOI:10.3892/mmr.2016.5469   (Journal Full-text)

MicroRNAs (miRNAs) act as tumor promoters or tumor suppressors in different human malignancies. In the current study, using an Agilent miRNA microarray, miR-30a was found to be a significantly downregulated miRNA in castration-resistant prostate cancer (CRPC) tissues, compared with androgen-dependent prostate cancer tissues. Aberrant expression of cyclin E2 (CCNE2) has been reported in a variety of types of cancer including prostate cancer, and correlates with clinical outcome. The purpose of the current study was to determine the functions of miR-30a in CRPC cell lines and identify whether CCNE2 was regulated by miR-30a. To analyze the associations between miR-30a and CCNE2 expression levels, pathological specimens were collected, and reverse transcription-quantitative polymerase chain reaction and immunohistochemical staining were conducted. The effect of miR-30a overexpression on CRPC cell lines and the predicted target gene, CCNE2, were evaluated by MTT assay, flow cytometry, tumor formation, luciferase reporter assay and western blotting. miR-30a overexpression resulted in a significant suppression of cell growth in vitro, and reduced tumorigenicity in vivo. miR-30a repressed the expression of CCNE2 through binding to its 3'-untranslated region. CCNE2 was observed to be overexpressed in patients with CRCP and had an approximately inverse correlation with the level of miR-30a. The results suggest that miR-30a may function as a novel tumor suppressor in CRPC. Its anti-oncogenic activity may occur by the reduced expression of a distinct cell cycle protein, CCNE2.




  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
CCNE2Humancastration-resistant prostate carcinoma treatmentIDA  RGD 
Ccne2Ratcastration-resistant prostate carcinoma treatmentISOCCNE2 (Homo sapiens) RGD 
Ccne2Mousecastration-resistant prostate carcinoma treatmentISOCCNE2 (Homo sapiens) RGD 


Genes (Rattus norvegicus)
Ccne2  (cyclin E2)

Genes (Mus musculus)
Ccne2  (cyclin E2)

Genes (Homo sapiens)
CCNE2  (cyclin E2)

Gene ATF4 activating transcription factor 4 Homo sapiens
Gene Atf4 activating transcription factor 4 Mus musculus
Gene Atf4 activating transcription factor 4 Rattus norvegicus