Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.10.2 (
focal adhesion kinase
)
44,029
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
More and more studies have reported that dysregulation of microRNAs (miRNAs) leads to the proliferation and
EMT
of multiple cancers. Recently, several reports have demonstrated that dysregulation of miR-4262 occurs in numerous cancers. However, its role and precise mechanism in human cervical cancer (CC) have not been well clarified. Hence, this study aimed to explore the biological roles and precise mechanisms of miR-4262 in CC cell lines. The level of miR-4262 was found to be significantly decreased in CC tissues and cell lines. Moreover, decreased expression of miR-4262 was closely related to increased expression of Kaiso (
ZBTB33
), which belongs to the BTB/POZ family, in CC tissues and cell lines. The proliferation and
EMT
of CC cells were inhibited by a miR-4262 mimic. However, downregulation of miR-4262 enhanced the proliferation and
EMT
of CC cells. Next, bioinformatics analysis predicted that miR-4262 might directly target the Kaiso gene. Besides, luciferase reporter assay had confirmed this result. Moreover, introduction of Kaiso in CC cells partially blocked the effects of miR-4262 mimic. In conclusion, miR-4262 suppressed the proliferation and
EMT
of CC cells by directly downregulating Kaiso.
...
PMID:Upregulation of MicroRNA-4262 Targets Kaiso (ZBTB33) to Inhibit the Proliferation and EMT of Cervical Cancer Cells. 2880 Jul 84
Aberrant extra-vascular expression of VE-cadherin (VEC) has been observed in metastasis associated with vasculogenic mimicry (VM); however, the ultimate reason why non-endothelial VEC favors the acquisition of this phenotype is not established. In this study, we show that human malignant melanoma cells have a constitutively high expression of phoshoVEC (pVEC) at Y658; pVEC is a target of
focal adhesion kinase
(
FAK
) and forms a complex with p120-catenin and the transcriptional repressor
kaiso
in the nucleus.
FAK
inhibition enabled
kaiso
to suppress the expression of its target genes and enhanced
kaiso
recruitment to KBS-containing promoters. Finally we have found that ablation of
kaiso
-repressed genes WNT11 and CCDN1 abolished VM. Thus, identification of pVEC as a component of the
kaiso
transcriptional complex establishes a molecular paradigm that links
FAK
-dependent phosphorylation of VEC as a major mechanism by which ectopical VEC expression exerts its function in VM.
...
PMID:VE-cadherin promotes vasculogenic mimicry by modulating kaiso-dependent gene expression. 2978 69
