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Target Concepts:
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Query: UMLS:C0029463 (
osteosarcoma
)
16,637
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
Previous studies have determined that long non-coding RNA (lncRNA)
Fer-1-like protein 4
(
FER1L4
) is suppressed in
osteosarcoma
(OS) and inhibits the tumorigenesis in a variety of cancer. However, the precise biological of
FER1L4
in OS has not been cleared. The aim of this study is to investigate the roles and potential mechanisms of
FER1L4
in apoptosis and epithelial-mesenchymal transition (EMT) in OS. In the present study, the levels of
FER1L4
were decreased significantly in OS tissues and cell lines compared with non-tumorous tissues or hFOB1.19. Knockdown of
FER1L4
in OS cells decreased the apoptosis rate, but increased the OS cell proliferation, upregulated the expression levels of CD133 and Nanog, as well as promoted Twist1 expression, increased the N-cadherin and Vimentin expression. In turn, the opposite trends were observed upon overexpression of
FER1L4
. In addition, the expression of PI3K, p-AKT (Ser470) and p-AKT (Thr308) was upregulated by siFER1L4, while decreased upon overexpression of
FER1L4
. MicroRNA (miRNA) -18a-5p, an
osteosarcoma
-promoting miRNA which was suggested a target of
FER1L4
in
osteosarcoma
, was identified to be a functional target of
FER1L4
on the regulating of cell apoptosis and EMT, presently. The effects of
FER1L4
overexpression on the markers of cell apoptosis, proliferation, EMT, and stemness and PI3K/AKT signaling were all reversed by miR-18a-5p upregulation. Furthermore, the suppressor of cytokine signaling 5 (SOCS5) was confirmed a target gene of miR-18a-5p by luciferase gene reporter assay and SOCS5 suppression by miR-18a-5p attenuated the effects of
FER1L4
overexpression on the OS cells apoptosis and the expressed levels of PI3K, AKT, Twist1, N-cadherin and Vimentin. In conclusion, our data indicated thatthe overexpression of
FER1L4
promoted apoptosis and inhibited the EMT markers expression and PI3K/AKT signaling pathway activation in OS cells via downregulating miR-18a-5p to promote SOCS5.
...
PMID:LncRNA FER1L4 induces apoptosis and suppresses EMT and the activation of PI3K/AKT pathway in osteosarcoma cells via inhibiting miR-18a-5p to promote SOCS5. 3147 23
