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: UMLS:C0023473 (
chronic myeloid leukemia
)
18,916
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Chronic myeloid leukemia
(
CML
) is a blood cell cancer with increased proliferation of granulocytes. Signal transducers and activators of transcription 3 (STAT3) is an important regulator of
CML
. To investigate the possible downstream factors of STAT3 and gain more insight into
CML
-related pathways, this study focused on the superior cervical ganglia protein 10-like protein (
SCLIP
, or SCG 10-like protein) and analyzed the functions of the STAT3-
SCLIP
pathway. The effects of STAT3 phosphorylation on
SCLIP
expression were examined by western blotting. Specific small interfering RNA (siRNA) was then used to knockdown
SCLIP
in the
CML
cell line K562 and the expression changes of STAT3 and factors further downstream, namely Bcl-2 and cyclin E1, were detected by RT-qPCR. Cell viability and apoptosis were also analyzed following the knockdown of
SCLIP
. Results showed a positive association between the phosphorylation of STAT3 and the expression of
SCLIP
. Knockdown of
SCLIP
inhibited the viability and induced the apoptosis of K562 cells. Knockdown of
SCLIP
did not affect the expression of
STAT3
mRNA but downregulated the mRNA levels of
Bcl-2
and
cyclin E1
. In conclusion, the results indicate that
SCLIP
is a direct downstream factor of STAT3, regulates Bcl-2 and cyclin E1 and mediates the viability and apoptosis of
CML
cells. Consisting of at least these four factors, the STAT3-
SCLIP
pathway might play critical roles in the regulation of
CML
. These data provided a more profound understanding of
CML
-related pathways.
...
PMID:Expression and functions of the STAT3-SCLIP pathway in chronic myeloid leukemia cells. 2788 67
