Myo10 Reference Search Result - Rat Genome Database

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

Advanced Search (OLGA)

References search result for All species
(View Results for all Objects and Ontologies)

3 records found for search term Myo10

Refine Term:

Sort By:

All

Export

RGD ID	Title	Citation	Abstract	PubMed	Pub Date
11074956	Myo10 is required for neurogenic cell adhesion and migration.	Yu H, etal., In Vitro Cell Dev Biol Anim. 2015 Apr;51(4):400-7. doi: 10.1007/s11626-014-9845-z. Epub 2014 Dec 10.	Myosin X (Myo10), an untraditional member of myosin superfamily, is characterized as an actin-based molecular motor, which plays a critical role in diverse cellular motile events. Previous research by our group has found that Myo10 ... (more) influenced neuronal radial migration in developing neocortex, but the underlying mechanism is still largely unknown. In this study, we found that knockdown of endogenous Myo10 in a normal gonadotropin-releasing hormone (GnRH) neuronal cell line transfected with the large T antigen (NLT) induced the impairment of cell motility and orientation. In the wound healing assay, with the Golgi complex staining to display cell polarity, Myo10 knockdown cells were randomly oriented compared to the control. Furthermore, suppressing the expression of Myo10 decreased the ability of cell-matrix adhesion. N-cadherin, a calcium-dependent classical cell adhesion molecule, rescued the migration deficiency caused by Myo10 knockdown in cell aggregates and collagen gel assay. These results suggest that Myo10 is required for neurogenic cell migration through N-cadherin mediated cell adhesion.	25491426	2015-05-01
11538591	MiR-340 suppresses cell migration and invasion by targeting MYO10 in breast cancer.	Chen CP, etal., Oncol Rep. 2016 Feb;35(2):709-16. doi: 10.3892/or.2015.4411. Epub 2015 Nov 12.	Breast cancer is one of the most common malignant tumors among females, and can seriously affect the physical and mental health and even threaten the lives of women. Recently, research has demonstrated that microRNAs (miRNAs), as a new method of regulation, have been shown to have oncogenic and tumo ... (more) rsuppressive functions in human breast cancer. Detection of their expression may lead to the identification of novel markers for breast cancer. In the present study, we firstly detected miR340 expression and found lower expression of miR340 in 6 human breast cancer cell lines by using RTqPCR. Then by using wound healing assay and Transwell migration and invasion experiments, we focused on the role of miR-340 in the regulation of tumor cell migration and invasion, exploring the relationship between them. The results revealed that induction of miR340 expression was able to suppress tumor cell migration and invasion, whereas knockdown of miR340 expression promoted breast cancer cell migration and invasion. At the gene level, MYO10 (myosin X), as a direct miR340 target gene, mediated the cell migration and invasion. Finally, we verified our research further at the tissue specimen level and in animal experiments. In brief, miR340 plays an important role in breast cancer progression. Thus, miR340 may be further explored as a novel biomarker for breast cancer metastasis and prognosis, and potentially a therapeutic target.	26573744	2016-10-01
11087253	NF-kappaB-mediated miR-124 suppresses metastasis of non-small-cell lung cancer by targeting MYO10.	Sun Y, etal., Oncotarget. 2015 Apr 10;6(10):8244-54.	Recently, dysregulation of microRNAs plays a critical role in cancer metastasis. Here, an in vivo selection approach was used to generate highly aggressive NSCLC sub-cell lines followed by comparing the microRNAs expression using microarrays. miR-124 was notably deregulated in both highly invasiv ... (more) e sub-cell lines and node-positive NSCLC specimens. Over-expression of miR-124 robustly attenuated migration and metastatic ability of the aggressive cells. MYO10 was subsequently identified as a novel functional downstream target of miR-124, and was up-regulated in node-positive NSCLC tissues. Knockdown of MYO10 inhibited cell migration, whereas forced MYO10 expression markedly rescued miR-124-mediated suppression of cell metastasis. Additionally, we found an activated NF-kappaB-centered inflammatory loop in the highly aggressive cells leading to down-regulation of miR-124. These results suggest that NF-kappaB-regulated miR-124 targets MYO10, inhibits cell invasion and metastasis, and is down-regulated in node-positive NSCLC.	25749519	2015-06-01