| Title |
MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met
|
|---|---|
| Published in |
Tumor Biology, December 2014
|
| DOI | 10.1007/s13277-014-2917-6 |
| Pubmed ID | |
| Authors |
Yue Gao, Fan Zeng, Jia-Yan Wu, Hai-Yu Li, Jian-Jun Fan, Li Mai, Ji Zhang, Dong-Mei Ma, Yun Li, Fang-zhou Song |
| Abstract |
Metastasis is the leading cause of death in patients with breast cancer and aberrantly expressed microRNAs (miRNAs) are highly associated with this process. A previous study has shown that miR-335 is downregulated in breast cancer and can suppress tumor invasion and metastasis. Emerging evidences indicate that c-Met is implicated in cell scattering, migration, and invasion. However, little is known about the relationship between miR-335 expression and c-Met alteration in breast cancer. In the present study, we found that miR-335 expression was downregulated and c-Met protein expression was upregulated in two human breast cell lines. MiR-335 was found to negatively regulate c-Met protein level by directly targeting its 3' untranslated region (UTR). Forced expression of miR-335 decreased c-Met expression at protein levels and consequently diminished hepatocyte growth factor (HGF)-induced phosphorylation of c-Met and subsequently inhibited HGF promotion of breast cancer cell migration in a c-Met-dependent manner. MiR-335 expression was increased after 5-aza-2'-deoxycytidine (5-AZA-CdR) treatment, and 5-AZA-CdR treatment resulted in the same phenotype as the effect of miR-335 overexpression. Taken together, these results demonstrate that miR-335 suppresses breast cancer cell migration by negatively regulating the HGF/c-Met pathway. |
X Demographics
The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 23 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 23 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 6 | 26% |
| Student > Master | 5 | 22% |
| Researcher | 4 | 17% |
| Student > Bachelor | 2 | 9% |
| Other | 1 | 4% |
| Other | 2 | 9% |
| Unknown | 3 | 13% |
| Readers by discipline | Count | As % |
|---|---|---|
| Agricultural and Biological Sciences | 7 | 30% |
| Biochemistry, Genetics and Molecular Biology | 7 | 30% |
| Neuroscience | 2 | 9% |
| Medicine and Dentistry | 1 | 4% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 4% |
| Other | 0 | 0% |
| Unknown | 5 | 22% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 11 December 2014.
All research outputs
#20,246,428
of 22,774,233 outputs
Outputs from Tumor Biology
#1,834
of 2,622 outputs
Outputs of similar age
#302,547
of 361,216 outputs
Outputs of similar age from Tumor Biology
#99
of 158 outputs
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