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Query: UMLS:C0345904 (
liver cancer
)
15,188
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The tissue blood flow (TBF) of primary
liver cancer
and normal live in 54 rats were measured following infusion of vasoactive agents into the celiac axis under continuous recording of blood pressure.
Angiotensin II
(AT) (1.0 micrograms/kg/min) and Prostaglandin F2 alpha (PGF) (1.0 micrograms/kg/min) were used. The former increased TBF of the tumor and blood pressure and the latter reduced TBF of the tumor with no remarkable change of the blood pressure, but both drugs made little or no influence on TBF of the normal liver. Dibutyryl cyclic AMP (DBcAMP) (2.0 mg/kg/hr) infusion increased TBF of the both tumor and normal liver with no significant change of blood pressure. PGF (1.0 micrograms/kg/min) infusion after preinfusion of DBcAMP did not cause the decrease of TBF of the tumor.
...
PMID:[The hepatic hemodynamic response to intra-arterial infusion of vasoactive agents--Part 2. Blood flow measurements in rats with liver cancer]. 254 99
Increasing evidence suggests that the renin-angiotensin system (RAS) plays an important role in tumorigenesis. The interaction between
Angiotensin II
(AngII) and angiotensin type 1 receptor (AT1R) may have a pivotal role in hepatocellular carcinoma (HCC) and therefore, AT1R blocker and angiotensin I-converting enzyme (ACE) inhibitors may have therapeutic potential in the treatment of
hepatic cancer
. Although the involvement of AT1R has been well explored, the role of the angiotensin II Type 2 receptor (AT2R) in HCC progression remains poorly understood. Thus, the aim of this study was to explore the effects of AT2R overexpression on HCC cells in vitro and in mouse models of human HCC. An AT2R recombinant adenoviral vector (Ad-G-AT2R-EGFP) was transduced into HCC cell lines and orthotopic tumor grafts. The results indicate that the high dose of Ad-G-AT2R-EGFP-induced overexpression of AT2R in transduced HCC cell lines produced apoptosis. AT2R overexpression in SMMC7721 cells inhibited cell proliferation with a significant reduction of S-phase cells and an enrichment of G1-phase cells through changing expression of CDK4 and cyclinD1. The data also indicate that overexpression of AT2R led to apoptosis via cell death signaling pathway that is dependent on activation of p38 MAPK, pJNK, caspase-8 and caspase-3 and inactivation of pp42/44 MAPK (Erk1/2). Finally, we demonstrated that moderately increasing AT2R expression could increase the growth of HCC tumors and the proliferation of HCC cells in vivo. Our findings suggest that AT2R overexpression regulates proliferation of hepatocellular carcinoma cells in vitro and in vivo, and the precise mechanisms of this phenomenon are yet to be fully determined.
...
PMID:Effects of angiotensin II type 2 receptor overexpression on the growth of hepatocellular carcinoma cells in vitro and in vivo. 2439 21
Angiotensin II
type 1 receptor (AT1R) was reported to express in many types of tumors, promoting tumor growth and angiogenesis. We herein examined AT1R expression in
liver cancer
and the potential antitumor effects of AT1R antagonist Candesartan in
liver cancer
. We found that AT1R expression was positively correlated with VEGF-A expression and microvascular density (MVD) in 40
HCC
patients.
Angiotensin II
and Candesartan neither had effects on the proliferation of
liver cancer
cells in vitro. However,
Angiotensin II
upregulated AT1R protein expression and promoted production of VEGF-A in
liver cancer
cells in a dose-dependent manner. Candesartan was able to reverse this process in a dose-dependent manner. Moreover, Candesartan downregulated the expression of VEGF-A in SMMC-7721 bearing xenografts in mice and inhibited tumor growth and angiogenesis in vivo. Our data suggested that AT1R antagonist Candesartan might be useful to suppress
liver cancer
by inhibiting angiogenesis.
...
PMID:Candesartan attenuates angiogenesis in hepatocellular carcinoma via downregulating AT1R/VEGF pathway. 2747 May 71
Angiotensin II
(AngII) is an important factor that promotes the proliferation of cancer cells, whereas celastrol exhibits a significant antitumor activity in various cancer models. Whether celastrol can effectively suppress AngII mediated cell proliferation remains unknown. In this study, we studied the effect of celastrol on AngII-induced HepG2 cell proliferation and evaluated its underlying mechanism. The results revealed that AngII was able to significantly promote HepG2 cell proliferation via up-regulating AngII type 1 (AT
1
) receptor expression, improving mitochondrial respiratory function, enhancing nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, increasing the levels of reactive oxygen species (ROS) and pro-inflammatory cytokines. The excess ROS from mitochondrial dysfunction is able to cause the apoptosis of tumor cells via activating caspase3 signal pathway. In addition, the reaction between NO and ROS results in the formation of peroxynitrite (ONOO
-
), and then promoting cell damage. celastrol dramatically enhanced ROS generation, thereby causing cell apoptosis through inhibiting mitochodrial respiratory function and boosting the expression levels of AngII type 2 (AT
2
) receptor without influencing NADPH oxidase activity. PD123319 as a special inhibitor of AT
2
R was able to effectively decreased the levels of inflammatory cytokines and endothelial nitric oxide synthase (eNOS) activity, but only partially attenuate the effect of celastrol on AnII mediated HepG2 cell proliferation. Thus, celastrol has the potential for use in
liver cancer
therapy. ROS derived from mitochondrial is an important factor for celastrol to suppress HepG2 cell proliferation.
...
PMID:The ROS derived mitochondrial respirstion not from NADPH oxidase plays key role in Celastrol against angiotensin II-mediated HepG2 cell proliferation. 2765 84
