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:P42574 (
caspase-3
)
45,978
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Novel long non-coding RNA
Fer-1-like protein 4
(
FER1L4
) has been identified as a tumor suppressor in endometrial carcinoma, ovarian cancer, hepatocellular carcinoma, esophageal squamous cell carcinoma. However, the function of
FER1L4
in osteosarcoma has not been clear. The aim of the research was to explore the effects of
FER1L4
in osteosarcoma. Results showed that
FER1L4
was observed to be lowly expressed in osteosarcoma cell lines (US-O2, MG-63 and SaOS-2 cells), especially MG63 cells. Besides, overexpression of
FER1L4
remarkably repressed the proliferation, migration and invasion of MG63 cells.
FER1L4
-induced apoptotic cell death leaded to the activation of
caspase-3
and Bax/Bcl2. Moreover, epithelial-mesenchymal transition (EMT) was tremendously suppressed by increased
FER1L4
, evidences were the increased E-cadherin and reduced vimentin and fibronectin. Blocking
FER1L4
expression by sh-
FER1L4
treatment increased the expression of SOX9, CD44, ALDH1, Nanog and Oct4, indicating that
FER1L4
could effectively decrease cell stemness in osteosarcoma. Furthermore, the protein levels of p-AKT and p-PI3K were remarkably suppressed when
FER1L4
was knocked down. In conclusion, the study indicated that
FER1L4
acted as a tumor suppressor in osteosarcoma via activating PI3K/AKT pathway may be a new prognostic biomarker and potential therapeutic target for osteosarcoma intervention.
...
PMID:Overexpression of FER1L4 promotes the apoptosis and suppresses epithelial-mesenchymal transition and stemness markers via activating PI3K/AKT signaling pathway in osteosarcoma cells. 3100 Mar 82