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:C0699790 (
colon cancer
)
28,837
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Purpose:
We have previously reported that PRDX2 plays an oncogenic role in
colon cancer
. In this study, the mRNA expression profile of PRDX2 in HCT116 cells was investigated. Furthermore, we selected
Dynamin 3
(
DNM3
), which is up-regulated by siPRDX2, to investigate its expression pattern and functions in
colon cancer
.
Patients and methods:
PRDX2 siRNA was transfected into HCT116 cells and the mRNA profile was tested by RNA-Sequencing. The expression of interest proteins was determined by Western blot.
DNM3
expression in
colon cancer
tissues and para-carcinoma tissues was evaluated by Western blot and immunohistochemistry assays. Full-length cDNA of
DNM3
was cloned into pcDNA3.1 and introduced into HCT116 and HT29 cells. Cell proliferation was tested by CCK-8 and colony formation assays. Cell invasion and migration were tested by transwell assays. Gelatin zymography was utilized for detection of MMP9 activity. Cell apoptosis was investigated with Annexin V/PI staining and flow cytometry and visualized with Hoechst/PI staining assay. All statistical analysis was performed with SPSS 17.0 software.
Results:
PRDX2 knockdown led to 210 up-regulated genes and 16 down-regulated genes in HCT116 cells. We also found that
DNM3
expression was up-regulated following PRDX2 silencing in HCT116 and HT29 cells. In
colon cancer
patients,
DNM3
was down-regulated and showed a significant association with pathologic grading.
DNM3
overexpression inhibited cell proliferation and induced apoptosis in HCT116 and HT29 cells. Cell migration and invasion were also down-regulated in
DNM3
overexpressing
colon cancer
cells, which might be due to the inhibition of MMP9 proteolytic activities. After thorough investigation of the potential mechanism involved, we hypothesized that
DNM3
overexpression induced activation of the mitochondrial apoptosis pathway and inhibition of the AKT pathway.
Conclusion:
These data suggest that
DNM3
is down-regulated in
colon cancer
, serving as a tumor suppressor. Our study provides new sights into the prognostic value and therapeutic application of
DNM3
in
colon cancer
.
...
PMID:siPRDX2-elevated DNM3 inhibits the proliferation and metastasis of colon cancer cells via AKT signaling pathway. 3138 12