MiR‐455‐3p regulates early chondrogenic differentiation via inhibiting Runx2

Zhang, Zhiqi; Hou, Changhe; Meng, Fangang; Zhao, Xiaoyi; Zhang, Ziji; Huang, Guangxin; Chen, Weishen; Fu, Ming; Liao, Weiming

doi:10.1016/j.febslet.2015.09.032

Cited by 43 publications

(42 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[16][17][18][19] Recently, the miR-17-5p has been reported to be associated with tumor progression and metastasis via targeting multiple signaling pathways, such as the Wnt/β-catenin and MAPK signaling pathways. [16][17][18][19] Recently, the miR-17-5p has been reported to be associated with tumor progression and metastasis via targeting multiple signaling pathways, such as the Wnt/β-catenin and MAPK signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

miR‐17‐5p promotes proliferation and epithelial‐mesenchymal transition in human osteosarcoma cells by targeting SRC kinase signaling inhibitor 1

Zhao

Sun

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

MicroRNA‐17‐5p (miR‐17‐5p) and epithelial‐mesenchymal transition (EMT) have been reported to participate in the development and progression of multiple cancers. However, the relationship between the miR‐17‐5p and EMT in osteosarcoma (OS) is still poorly understood. This study was to investigate the effects of the miR‐17‐5p and its potential mechanism in regulating proliferation, apoptosis, and EMT of human OS. Quantitative real‐time PCR was used to detect the miR‐17‐5p and SRC kinase signaling inhibitor 1 (SRCIN1) messenger RNA expression in OS specimens and cell lines. After transfection with miR‐17‐5p inhibitors, proliferation, apoptosis, migration, and invasion of OS cells were assessed by using the Cell Counting Kit‐8, the annexin V‐FITC apoptosis, wound‐healing, and transwell assays. The SRCIN1 was validated as a target of the miR‐17‐5p through bioinformatics algorithms and luciferase reporter assay. Moreover, the expression of EMT markers, E‐cadherin, N‐cadherin, and Snail was identified by the Western blot analysis. MiR‐17‐5p was significantly upregulated in OS tumor samples and cell lines. It inhibited proliferation and EMT, and promoted apoptosis in OS. The SRCIN1 was identified as a direct target of the miR‐17‐5p. Silenced miR‐17‐5p could change the expression of EMT markers, such as upregulating the expression of E‐cadherin, and downregulating the expression of N‐cadherin and Snail through targeting the antioncogenic SRCIN1. These findings suggest that the miR‐17‐5p promotes cell proliferation, and EMT in human OS by directly targeting the SRCIN1, and reveal a branch of the miR‐17‐5p/SRCIN1/EMT signaling pathway involved in the progression of OS.

show abstract

Section: Discussionmentioning

confidence: 99%

miR‐17‐5p promotes proliferation and epithelial‐mesenchymal transition in human osteosarcoma cells by targeting SRC kinase signaling inhibitor 1

Zhao

Sun

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…By bioinformatics methods, we found the miR-455 might specifically bind to 3′UTR of HDAC2 gene. miR-455, which locates at the protein-coding gene Col27a1, has been reported to be involved in early chondrogenic differentiation regulation (30), down-regulation of MMP-9 during exercise (31), hypoxia signaling (32) and acquired temozolomide resistance in glioblastoma cells (33). However, investigations focused on the association between miR-455 and CRC are very few.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-455 suppresses the oncogenic function of HDAC2 in human colorectal cancer

Mao

Zhang

Zhao

et al. 2017

Braz J Med Biol Res

View full text Add to dashboard Cite

Colorectal cancer (CRC) is the fourth leading cause of cancer-induced mortality. Histone deacetylase 2 (HDAC2) is involved in prognosis and therapy of CRC. This study aimed to explore novel therapeutic targets for CRC. The alteration of HDAC2 expression in CRC tissues was estimated by qRT-PCR. After lentivirus transfection, HDAC2 knockdown was confirmed by western blot analysis. The effect of HDAC2 knockdown on cell proliferation was then assessed by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Screened by TargetScan, microRNA (miR)-455 was predicted to bind to 3 0 UTR of HDAC2 and the prediction was verified by luciferase assay. Finally, cells were transfected, respectively, with miR-455 mimics or miR-455 negative control (miR-NC) and the expression of HDAC2, cell proliferation and apoptosis of transfected cells were respectively evaluated by western blot analysis, MTT assay and flow cytometry. Results showed that the HDAC2 expression was up-regulated in CRC tissues (Po0.05). HDAC2 knockdown significantly decreased cell viability at day 3 (Po0.05), day 4 (Po0.01), and day 5 (Po0.001) after infection. Then, miR-455 was verified to directly target HDAC2, resulting in a significant difference in luciferase activity (Po0.01). Moreover, miR-455 decreased the expression of HDAC2 (Po0.01). miR-455 remarkably decreased cell viability at day 3 (Po0.05), day 4 (Po0.01), and day 5 (Po0.001) after transfection while inducing cell apoptosis (Po0.001). In conclusion, miR-455 inhibited cell proliferation while inducing cell apoptosis by targeting HDAC2 in CRC cells.

show abstract

“…Guled [34] showed that miR-455-3p was up-regulated in smoker group of malignant mesothelioma patients compared with non-smoker group. Zhang et al [35] revealed that miR-455-3p functioned as an activator for early chondrogenic differentiation by inhibiting the expression of Runt-related transcription factor 2 (Runx2). Moreover, miR-455-3p was found to be linked with acquired temozolomide resistance in glioblastoma multiforme cells [36].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-455-3p promotes invasion and migration in triple negative breast cancer by targeting tumor suppressor EI24

Meng

Pan

et al. 2016

Oncotarget

View full text Add to dashboard Cite

Lacking of treatment methods for the patients with triple negative breast cancer (TNBC) underscores the pivotal needs to further understand its biology as well as to find better biomarkers and develop novel therapeutic strategies. Increasing evidences support that aberrantly expressed microRNAs (miRNAs) are involved in tumorigenesis and may serve as biomarkers for diagnostic and prognostic purposes of various cancers. In current study, we found that miR-455-3p and miR-196a-5p were intensively overexpressed in TNBC compared with the hormone receptor (HR) positive breast cancer whereas miR-425-5p was down-regulated by miRNA microarray analysis. qRT-PCR analysis confirmed that the expression of miR-455-3p in TNBC cell lines MDA-MB-231 and MDA-MB-468 was higher than that in HR positive breast cancer cell line MCF-7(p<0.01). Functional experiments in vitro showed that miR-455-3p enhanced cell proliferative, invasive and migrational abilities in TNBC cell lines. miRNA targets prediction showed SMAD2, LTBR and etoposide induced 2.4 (EI24) were potential target genes of miR-455-3p, and then it was confirmed by qRT-PCR assay. Dual luciferase reporter assay showed the specific binding of miR-455-3p to 3′ UTR of EI24 in TNBC. Then we found miR-455-3p inhibited the EI24 expression at the levels of mRNA and protein. Through small interfering RNA (siRNA) targeting EI24 gene, there were strengthened capabilities of invasion and migration of TNBC cells, and increased expression of EI24 had the inverse effects. In conclusion, the data suggest that miRNA455-3p promotes invasion and migration by targeting tumor suppressor EI24 and might be a potential prognostic biomarker and therapeutic target in TNBC.

show abstract

MiR‐455‐3p regulates early chondrogenic differentiation via inhibiting Runx2

Cited by 43 publications

References 41 publications

miR‐17‐5p promotes proliferation and epithelial‐mesenchymal transition in human osteosarcoma cells by targeting SRC kinase signaling inhibitor 1

miR‐17‐5p promotes proliferation and epithelial‐mesenchymal transition in human osteosarcoma cells by targeting SRC kinase signaling inhibitor 1

MicroRNA-455 suppresses the oncogenic function of HDAC2 in human colorectal cancer

MicroRNA-455-3p promotes invasion and migration in triple negative breast cancer by targeting tumor suppressor EI24

Contact Info

Product

Resources

About