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: UNIPROT:P05412 (
c-Jun
)
11,453
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1), a long non-coding RNA transcribed from the antisense strand of protein coding gene AFAP1, has attracted attention in cancer research. Despite, its biological function and regulatory mechanism in hepatocellular carcinoma still unknown. The present study revealed AFAP1-
AS1
mediated hepatocarcinoma progression through targeting CRKL. The bidirectional interaction of AFAP1-
AS1
and oncogenic protein CRKL, and the deregulation of AFAP1-
AS1
effects on Ras, MEK and
c-Jun
activities were investigated in depth. AFAP1-
AS1
was upregulated in surgical tumorous tissues from hepatocarcinoma patients compared with the paired paracancerous non-tumor liver tissues, and in hepatocarcinoma Huh7, HCCLM3 and HepG2 cell lines compared with LO2, a normal liver cell line. AFAP1-
AS1
knockdown noticeably suppressed the proliferative, migratory and invasive properties, and the epithelial-mesenchymal transition (EMT) process of HepG2 and HCCLM3 through upregulating E-cadherin and downregulating N-cadherin and vimentin. CRKL knockdown reduced AFAP1-
AS1
expression levels in HepG2 and HCCLM3 cells. AFAP1-
AS1
suppression impaired CRKL expression in HepG2 and HCCLM3. AFAP1-
AS1
level change was positively correlated with the expression level changes of Ras, MEK and
c-Jun
in mediating the invasiveness of hepatocarcinoma cells. Current work demonstrated AFAP1-
AS1
to be an applicable progression indicator of hepatocarcinoma. AFAP1-
AS1
probably promotes the proliferation, EMT progression and metastasis of hepatocarcinoma cells
via
CRKL mediated Ras/MEK/
c-Jun
and cadherin/vimentin signaling pathways. AFAP1-
AS1
-CRKL bidirectional feedback signaling is worthy of further study on the monitoring, diagnosis and treatment of cancers.
...
PMID:Bidirectional interaction of lncRNA AFAP1-AS1 and CRKL accelerates the proliferative and metastatic abilities of hepatocarcinoma cells. 3228 May 42