Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Enzyme
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Query: UMLS:C1864663 (
HCC
)
2,985
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The aim of the present study was to investigate the correlation of STAT3 and AKT in
HCC
cells.
HCC
cells were transfected with si-STAT3 and si-
AKT2
in vitro
and the mRNA expression of STAT3 and AKT was detected by RT-PCR, and the protein expression was measured by western blot. MTT assays were used to evaluate cell proliferation, and Transwell assays were performed to detect the ability of migration and invasion. The relationship between STAT3 and AKT was analyzed by ChIP and Dual-luciferase reporter (DLR) assays. A nude mice experiment was used to verify the correlation. In the present study, we found that the expression of p-
AKT2
and its downstream molecules were reduced in
HCC
cells transfected with si-STAT3, and the expression of p-STAT3 and its downstream molecules was decreased in
HCC
cells transfected with si-
AKT2
. Moreover, the ability of
HCC
cells proliferation, migration and invasion was decreased in si-STAT3 transfection group, but
AKT2
reversed the role of si-STAT3 in
HCC
cells. The ChIP experiment found that STAT3 could bind to the
AKT2
promoter in
HCC
cells. The DLR assay showed that the luciferase activity of
AKT2
promoter was enhanced in
HCC
cells treated by IL-6. The nude mice experiment found that the tumor grew slowly after transfection with the STAT3-siRNA lentiviral vector, while
AKT2
reversed the effect. STAT3 and
AKT2
had mutual regulatory relationship, and STAT3 promoted the occurrence and development of
HCC
by regulating
AKT2
.
...
PMID:STAT3 promotes the proliferation and migration of hepatocellular carcinoma cells by regulating AKT2. 2943 76
Nuclear-enriched RNA-binding proteins (RBPs) are mainly involved in transcriptional regulation, which is a critical checkpoint to tune gene diversity and expression levels. We analyzed nuclear RBPs in human
HCC
tissues and matched normal control tissues. Based on the gene expression levels, PTBP3 was identified as top-ranked in the nuclei of
HCC
cells.
HCC
cell lines then were transfected with siRNAs or lentiviral vectors. PTBP3 promoted
HCC
cell proliferation and metastasis both in vitro and in vivo. RNA immunoprecipitation (RIP), fluorescence in situ hybridization (FISH) and qRT-PCR assays verified that PTBP3 protein recruited abundant lnc-NEAT1 splicing variants (NEAT1_1 and NEAT1_2) and pre-miR-612 (precursor of miR-612) in the nucleus. NEAT1_1, NEAT1_2 and miR-612 expression levels were determined by PTBP3. Correlational analyses revealed that PTBP3 was positively correlated with NEAT1, but it was inversely correlated with miR-612 in
HCC
. The P53/CCND1 and
AKT2
/EMT pathways were determined by NEAT1 and miR-612 respectively in
HCC
. The PTBP3
high
and NEAT1
high
/miR-612
low
patients had a shorter overall survival. Therefore, nuclear-enriched RBP, PTBP3, promotes
HCC
cell malignant growth and metastasis by regulating the balance of splicing variants (NEAT1_1, NEAT1_2 and miR-612) in
HCC
.
...
PMID:PTBP3 splicing factor promotes hepatocellular carcinoma by destroying the splicing balance of NEAT1 and pre-miR-612. 3006 40
