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:C0345904 (
liver cancer
)
15,188
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We have applied our method for the simultaneous detection of plasma
ubiquinol
-10 (reduced form) and ubiquinone-10 (oxidized form) (S. Yamashita and Y. Yamamoto, Anal. Biochem. 250, 66-73, 1997) to plasmas of normal subjects (n = 16) and patients with chronic active hepatitis (n = 28), liver cirrhosis (n = 16), and hepatocellular carcinoma (n = 20) to evaluate the pressure of oxidative stress in these patients. The average ubiquinone-10 percentages (+/- S.D.) in total ubiquinone-10 and
ubiquinol
-10 in the four groups were 6.4 +/- 3.3, 12.9 +/- 10.3, 10.6 +/- 6.8, and 18.9 +/- 11.1, respectively, indicating a significant increase in ubiquinone-10 percentage in patient groups in comparison to normal subjects. These results and a significant decrease in the plasma ascorbate level in patient groups indicate that oxidative stress is evident after the onset of hepatitis and the subsequent cirrhosis and
liver cancer
.
...
PMID:Oxidative stress in patients with hepatitis, cirrhosis, and hepatoma evaluated by plasma antioxidants. 963 73
Ubiquinol
cytochrome c reductase binding protein (UQCRB) is known to play crucial roles in the development of various types of diseases. However, the link between UQCRB and microRNAs remains unknown. In the present study, we performed microRNA sequencing of mutant UQCRB-expressing stable cell lines that exhibited pro-oncogenic activities caused by expression of the mutant UQCRB gene. Results showed that hsa-miR-10a-5p was significantly downregulated in the mutant UQCRB-expressing cell lines. Furthermore, mRNA sequencing and gene ontology analysis of differentially expressed genes (DEGs) revealed that the cholesterol biosynthesis pathway might be activation by mutant UQCRB expression. Moreover, inhibition of cholesterol synthesis in mutant UQCRB-expressing cells via treatment with the specific inhibitors suppressed the cell proliferation. Transfection with a hsa-miR-10a-5p mimic validated that lanosterol synthase (LSS) is a target of hsa-miR-10a-5p. In addition, hsa-miR-10a-5p was found to be downregulated in
liver cancer
cell lines overexpressing UQCRB. Taken together, our findings highlighted the potential use of hsa-miR-10a-5p as a biomarker for UQCRB related diseases.
...
PMID:Hsa-miR-10a-5p downregulation in mutant UQCRB-expressing cells promotes the cholesterol biosynthesis pathway. 3012 Mar 11
Coenzyme Q
10
(CoQ
10
) is an essential factor in the mitochondrial respiratory chain and is closely associated with ATP production in humans. It is known that orally administered CoQ
10
in humans is rapidly reduced, and most is detected as a reduced form,
ubiquinol
-10 (CoQ
10
H
2
), in serum. However, the mechanism of exogenous CoQ
10
reduction in vivo is unclear. Therefore, in order to clarify how CoQ
10
is reduced to CoQ
10
H
2
, we conducted a study using human
liver cancer
cell line Hep G2 cells, which show strong intracellular CoQ
10
-reducing activity. When intact cells were incubated with CoQ
10
, the exogenously added CoQ
10
was incorporated into the cells, time-, concentration-, and temperature-dependently, and 50-80% of that was detected as CoQ
10
H
2
. On the other hand, a part of the extracellular CoQ
10
was also detected as CoQ
10
H
2
, and the amount was greater than that of the intracellular CoQ
10
H
2
. Furthermore, the CoQ
10
-loaded cells did not leak the intracellular CoQ
10
H
2
(or CoQ
10
) to the outside of the cells, and modulation of the extracellular CoQ
10
H
2
amount had little effect on the intracellular CoQ
10
or CoQ
10
H
2
contents, suggesting the existence of an individual mechanism of CoQ
10
reduction inside and outside the cells. Moreover, intact cells could reduce CoQ
10
in low-density lipoprotein to CoQ
10
H
2
. Therefore, we concluded that a novel CoQ
10
-reducing mechanism may exist in the plasma membrane, probably the outer surface, of Hep G2 cells, and it may work to reduce extracellular CoQ
10
and/or maintain extracellular CoQ
10
H
2
.
...
PMID:Extracellular coenzyme Q
10
(CoQ
10
) is reduced to ubiquinol-10 by intact Hep G2 cells independent of intracellular CoQ
10
reduction. 3140 Mar 2
