Search Result

Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune	T-cell	Survival
Enhancer		Apoptosis		Drug	fludarabine
Variant		Cell Growth		Circulating	2
MiRNA		EMT		Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	breast cancer
ICD-0-3	C50
Methods	Microarray, qPCR
Sample	breast cancer tissues, cell lines (MCF7, ZR75-1, SKBR3, MDA-231, 231BrM)
Expression Pattern	down-regulated
Function Description	we profiled long noncoding RNAs in brain metastatic tumors from patients with breast cancer and found that the X-inactive-specific transcript (XIST) was significantly downregulated in these tissues. knockout of XIST in mice mammary glands accelerated primary tumor growth as well as metastases in the brain. Decreased expression of XIST stimulated epithelial-mesenchymal transition and activated c-Met via MSN-mediated protein stabilization, Loss of XIST also augmented secretion of exosomal miRNA-503, which triggered M1-M2 polarization of microglia. This M1-M2 conversion upregulated immune suppressive cytokines in microglia that suppressed T-cell proliferation. In addition, fludarabine was found to be highly selective for cells with low levels of XIST expression as it showed selective inhibition of 231BrM and SKBrM3 cells, compared with SKBR3, MCF7, and ZR75-1 cells, which have high levels of XIST. We also examined the relationship between miR-503 expression and relapse-free survival in patients with breast cancer using the GSE22220 database and found that a higher expression of miR-503 was negatively correlated with the relapse-free survival.
Pubmed ID	30026327
Year	2018
Title	Loss of XIST in Breast Cancer Activates MSN-c-Met and Reprograms Microglia via Exosomal miRNA to Promote Brain Metastasis.

External Links