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)
Oxaliplatin is widely used for chemotherapy of several malignancies, especially of
colon cancer
. As the mechanism of resistance to oxaliplatin is unclear, we established an oxaliplatin-resistant cell line, THC8307/L-OHP, from an oxaliplatin-sensitive colonic cancer cell line, THC8307. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium assay indicated that THC8307/L-OHP has 30.99-fold greater resistance to oxaliplatin than THC8307. Analyzing its gene expression profile using an in-house oligomicroarray, a number of genes were differentially expressed in the THC8307/L-OHP cells, compared with parental cells (THC8307). Proapoptotic genes such as
STK17A
and BNIP3 were significantly downregulated, whereas the genes PSAP and GDIA1, which were involved in antiapoptosis, were overexpressed. Moreover, the THC8307/L-OHP cells are also resistant to the other anticancer drug 5-fluorouracil, and the expression levels of the differentially regulated genes such as S100P, CAeta, STA15, TCF8 are constantly maintained. These results provide clues for understanding the oxaliplatin-resistant mechanisms and imply markers to predict drug sensitivities for 'personalized chemotherapy'.
...
PMID:Establishment and gene analysis of an oxaliplatin-resistant colon cancer cell line THC8307/L-OHP. 1776 91
Ovarian cancer is the main cause of cancer mortality in gynecological tumors around the world. Drug resistance to a variety of chemotherapeutics continue to be one of the main causes of treatment failure. In a previous study, it was demonstrated that
STK17A
, a proapoptotic gene, was significantly downregulated in acquired resistance phenotypes of
colon cancer
cells that are resistant to oxaliplatin and 5-fluorouracil. Therefore in the present study, the association between
STK17A
expression and ovarian cancer with initial drug resistance was investigated and the influence of STK17 on ovarian cancer cell proliferation and doubling time. In the present study, ovarian cancer cell lines that express low levels of
STK17A
were established by targeting
STK17A
with specific siRNA. In addition, up-regulation of
STK17A
was established in ovarian cells by pCDNA3flu/
STK17A
. The sensitivity of the transfected cells and controls to paclitaxel, carboplatin was examined by MTT assay, and the levels of proliferation and apoptosis were analyzed by flow cytometry. In the cells that were transfected with siRNA resulting in reduced expression of
STK17A
, the 50% inhibitory concentration (IC
50
) of the chemotherapy drugs paclitaxel and carboplatin was increased compared with control cells (P<0.05). By contrast, in the cells that overexpressed
STK17A
following treatment with pCDNA3flu/
STK17A
, the IC
50
of the chemotherapy drugs reduced in each case, and was significantly lower compared with the control (P<0.05). There was a variable susceptibility to carboplatin and paclitaxel resulting from altering the levels of
STK17A
expression in ovarian cancer cell lines. The growth of
STK17A
/siRNA transfected cells was promoted compared with that of the control cells and accordingly their cell doubling time was shortened.
...
PMID:Effect of STK17A on the sensitivity of ovarian cancer cells to paclitaxel and carboplatin. 2744 2
