RefCirc
a reference database for circRNAs validated by experiments

circRNA-MYLK Details
Basic Information
circRNA    circRNA-MYLK
Alias    -
circBase ID    -
Host gene    MYLK
Species    homo sapiens
Peptide    -
Sequence  -
Expression
Description  circRNA-MYLK and VEGFA were significantly up-regulated and co-expressed in BC.
Method    microarray, qRT-PCR
Sample    bladder carcinomas and matched para-carcinomas, EJ, T24, 5673 and BIU-87
Function
Description  circRNA-MYLK levels were related to the progression of stage and grade of BC. Ectopically expressing circRNA-MYLK accelerated cell proliferation, migration, tube formation of HUVEC and rearranged cytoskeleton. Moreover, up-regulating circRNA-MYLK promoted epithelial-mesenchymal transition (EMT). Whereas circRNA-MYLK knockdown decreased cell proliferation, motility, and induced apoptosis. Finally, up-regulating circRNA-MYLK promoted the growth, angiogenesis and metastasis of BC xenografts.
Method    gain of function, loss of function
in vitro    EJ and T24 cells
in vivo    4-week-old male BALB/c mice
Interaction
Target    miR-29a
Type    circRNA-miRNA
Sample    293T, EJ
Experiment    AGO2 RIP, luciferase reporter assay, RNA FISH
Description    circRNA-MYLK pulled down with Anti-Ago2 antibodies was significantly enriched in cells transfected with miR-29a mimics compared to controls. circRNA-MYLK and miR-29a are colocalized in BC tissues and cells using FISH. Upregulation of miR-29a could remarkably reduce the luciferase activities of WT reporter but not the Mutant one, suggesting that miR-29a could interact with circRNA-MYLK via complementary seed region.
ceRNA target    VEGFA
Reference
Pubmed ID    28687357
Trait/Disease    Bladder Cancer
Title    Circular RNA MYLK as a competing endogenous RNA promotes bladder cancer progression through modulating VEGFA/VEGFR2 signaling pathway.
Authors    Zhong Z, Huang M, Lv M, He Y, Duan C, Zhang L, Chen J.
Journal    Cancer Lett. 2017