High expression of vanilloid receptor-1 is associated with better prognosis of patients with hepatocellular carcinoma

Miao, Xiangshui; Liu, Guoxing; Xu, Xundi; Xie, Chengzhi; Sun, Fadi; Yang, Yaohui; Zhang, Tao; Hua, Shucheng; Fan, Wentao; Li, Qinglong; Huang, Shengfu; Qun-wei, Wang; Li, Guoli; Zhong, Di

doi:10.1016/j.cancergencyto.2008.05.011

Cited by 52 publications

(41 citation statements)

References 40 publications

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“…Our previous study showed that chronic dietary capsaicin reduces weight gain in mice [25]. TRPV1 is also expressed in hepatocytes and livers [10,21], but its function is unknown. Our data confirmed that chronic dietary capsaicin reduced the hepatic triglyceride and prevented fatty liver.…”

Section: Discussionmentioning

confidence: 99%

“…Transient receptor potential vanilloid 1 (TRPV1) is able to sense a plethora of endogenous physical and chemical stimuli and transduce noxious heat and painful stimuli [12][13][14]26]. Functional TRPV1 has also been found in hepatic cells and upregulation of TRPV1 predicts a better prognosis for patients with hepatocellular carcinomas [10]. Uncoupling protein 2 (UCP2) was reported to play a role in hepatic lipid metabolism, mitochondrial bioenergetics, oxidative stress, and apoptosis [1].…”

Section: Introductionmentioning

confidence: 99%

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TRPV1 activation prevents nonalcoholic fatty liver through UCP2 upregulation in mice

Chen

et al. 2012

Pflugers Arch - Eur J Physiol

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Nonalcoholic fatty liver is characterized by the fatty deformation and lipid deposition of hepatic parenchymal cells that are associated with cardiometabolic diseases. In this study, we report the effect of capsaicin on its receptor, transient receptor potential vanilloid 1 (TRPV1) cation channel, in preventing fatty liver formation. Functional TRPV1 has been detected in hepatocytes and liver tissues. TRPV1 activation by capsaicin reduced lipid accumulation and triglyceride level in the liver from wild-type (WT) mice. However, these effects were absent in the liver from TRPV1(-/-) mice. Chronic dietary capsaicin increased the hepatic uncoupling protein 2 (UCP2) expression in WT but not in TRPV1(-/-) mice (P < 0.01). We conclude that TRPV1 long-time activation might prevent high-fat diet-induced fatty liver in mice through upregulation of hepatic UCP2. Dietary capsaicin may represent a promising intervention in populations at high risk for fatty liver.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

TRPV1 activation prevents nonalcoholic fatty liver through UCP2 upregulation in mice

Chen

et al. 2012

Pflugers Arch - Eur J Physiol

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“…Extracellular protons can be detected by G-protein-coupled receptors such as OGR1 or GPR4 [72,111]. [79] and, being a target for pain relief, their chronic blockade probably increases the risk for skin carcinogenesis [7,79]. On the other hand, TRPV1 activation by capsaicin promotes migration of human hepatoblastoma cells that were pretreated with hepatocyte growth factor [146].…”

Section: Ph Sensing In Tumor Cellsmentioning

confidence: 98%

Protons make tumor cells move like clockwork

Stock

Schwab

2009

Pflugers Arch - Eur J Physiol

213

226

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Cancer accounts for 13% of the yearly total mortality worldwide. Most cancer deaths are the sequel of metastatic diseases rather than of primary tumor growth. Thus, the major challenge in tumor therapy is the tumor cells' ability to metastasize. The extent to which a tumor metastasizes correlates with the tumor cells' migratory activity. Tumor cell migration requires a coordinated formation and release of cell adhesion contacts, a controlled cytoskeletal dynamics, the digestion and reorganization of the extracellular matrix, and local ion and water transport across the plasma membrane. All of these operations depend on intracellular pH (pH(i)) and extracellular pH (pH(e)). Numerous H(+), HCO (3) (-) , and monocarboxylate transporters as well as different carbonic anhydrase isozymes have considerable impact on pH(i) and pH(e) which spotlights them as possible, potential targets for anticancer therapeutics. Especially in solid tumors whose vascularization is often not sufficient, tumor cells cope with hypoxia and the resulting glycolysis by overexpressing the Na(+)/H(+) exchanger NHE1, monocarboxylate transporters MCT1 and/or MCT4, and the carbonic anhydrase CA IX. NHE1, MCT, and CA IX activity lead to an acidification of the extracellular space in order to maintain the cytosolic pH homeostasis stable. The present article gives a review on how this characteristic, acidic tumor micro- and nanoenvironment controls tumor cell migration.

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“…TRPV1-immunoreactivity has been shown to be increased in all layers of the tongue epithelium of the patients with tongue squamous cell carcinoma [132]. A recent study has indicated that TRPV1 receptor expression has a role in the prediction of hepatocellular carcinoma [133]. Hepatocyte growth factor/scatter factor (HGF/SF) promotes cell migration by stimulating the activity of TRPV1 in human hepatoblastoma cells [33].…”

Section: Trpv1 and Cancermentioning

confidence: 99%

Disease-Related Changes in TRPV1 Expression and Its Implications for Drug Development

Premkumar¹,

Bishnoi²

2011

CTMC

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The transient receptor potential vanilloid 1 (TRPV1) channel has been a topic of great interest, since its discovery in 1997. It is a homotetrameric non-selective cation channel predominantly expressed in a population of sensory neurons and its involvement in different modalities of pain has been extensively studied. However, TRPV1 has also been shown to be expressed in non-sensory neurons and non-neuronal cells. TRPV1 is considered as a potential target for drug development, based on its tissue distribution and its role in physiological functions. Here, we summarize the evidences for disease-related alterations in TRPV1 expression and function and review the current perspectives for the therapeutic potential of TRPV1 agonists and antagonists in the treatment of a wide range of diseases.

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High expression of vanilloid receptor-1 is associated with better prognosis of patients with hepatocellular carcinoma

Cited by 52 publications

References 40 publications

TRPV1 activation prevents nonalcoholic fatty liver through UCP2 upregulation in mice

TRPV1 activation prevents nonalcoholic fatty liver through UCP2 upregulation in mice

Protons make tumor cells move like clockwork

Disease-Related Changes in TRPV1 Expression and Its Implications for Drug Development

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