[Show abstract][Hide abstract] ABSTRACT: Conventional anticancer therapies, such as chemo- and/or radio-therapy are often unable to
completely eradicate cancers due to abnormal tumor microenvironment, as well as increased
drug/radiation resistance. More effective therapeutic strategies for overcoming these obstacles are
urgently in demand. Aptamers, as chemical antibodies that bind to targets with high affinity and
specificity, are a promising new and novel agent for both cancer diagnostic and therapeutic applications.
Aptamer-based cancer cell targeting facilitates the development of active targeting in
which aptamer-mediated drug delivery could provide promising anticancer outcomes. This review
is to update the current progress of aptamer-based cancer diagnosis and aptamer-mediated active
targeting for cancer therapy in vivo, exploring the potential of this novel form of targeted cancer
[Show abstract][Hide abstract] ABSTRACT: The biomedical application of graphene quantum dots (GQDs) is a new emerging area. However, their safety data are still in scarcity to date. Particularly, the effect of GQDs on the immune system remains unknown. This study aimed to elucidate the interaction of GQDs with macrophages and the underlying mechanisms. Our results showed that GQDs slightly affected the cell viability and membrane integrity of macrophages, whereas GQDs significantly increased reactive oxygen species (ROS) generation and apoptotic and autophagic cell death with an increase in the expression level of Bax–Bad caspase 3, caspase 9, beclin 1, and LC3-I/II and a decrease in that of Bcl-2. Furthermore, low concentrations of GQDs significantly increased the expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-8, whereas high concentrations of GQDs elicited opposite effects on the cytokines production. SB202190, a selective inhibitor of p38 mitogen-activated protein kinase (MAPK), abolished the cytokine-inducing effect of GQDs in macrophages. Moreover, GQDs significantly increased the phosphorylation of p38 MAPK and p65, and promoted the nuclear translocation of nuclear factor-κB (NF-κB). Taken together, these results show that GQDs induce ROS generation, apoptosis, autophagy, and inflammatory response via p38MAPK and NF-κB mediated signaling pathways in THP-1 activated macrophages.
[Show abstract][Hide abstract] ABSTRACT: (Pro)renin receptor (PRR) is predominantly expressed in the distal nephron where it is activated by angiotensin II (AngII), resulting in increased renin activity in the renal medulla thereby amplifying the de novo generation and action of local AngII. The goal of the present study was to test the role of cycloxygenase-2 (COX-2) in meditating AngII-induced PRR expression in the renal medulla in vitro and in vivo. Exposure of primary rat inner medullary collecting duct (IMCD) cells to AngII induced sequential increases in COX-2 and PRR protein expression. When the cells were pretreated with a COX-2 inhibitor NS-398, Ang II-induced upregulation of PRR protein expression was almost completely abolished, in parallel with the changes in medium active renin content. The inhibitory effect of NS-398 on the PRR expression was reversed by adding exogenous PGE2. A 14-day AngII infusion elevated renal medullary PRR expression and active and total renin content in parallel with increased urinary renin, all of which were remarkably suppressed by the COX-2 inhibitor celecoxib. In contrast, plasma and renal cortical active and total renin content were suppressed by AngII treatment, an effect that was unaffected by COX-2 inhibition. Systolic blood pressure (SBP) was elevated with AngII infusion, which was attenuated by the COX-2 inhibition. Overall, the results obtained from in vitro and in vivo studies have established a crucial role of COX-2 in mediating upregulation of renal medullary PRR expression and renin content during AngII hypertension.
[Show abstract][Hide abstract] ABSTRACT: Recently, it has been found that Fructus Schisandra Chinensis (FSC), a Chinese herbal medicine, and its related compounds have a profound impact on lipid metabolism process. FSC can be divided into two parts, i.e., seed and pulp. The current study aimed to examine the effect of aqueous extracts of FSC pulp (AqFSC-P) on serum/hepatic lipid and glucose levels in mice fed with a normal diet (ND) or a high cholesterol/bile salt diet (HCBD).
The AqFSC-P used in the present study was fractionated into supernatant (SAqFSC-P) and precipitate (PAqFSC-P) separated by centrifugation. Male ICR mice were fed with ND or HCBD, without or with supplementation of 1%, 3%, or 9% (w/w) SAqFSC-P or PAqFSC-P for 10 days. Biomarkers were determined according to the manufacturer's instruction.
Supplementation with SAqFSC-P or PAqFSC-P significantly reduced serum and hepatic triglyceride levels (approximately 40%) in ND- and/or HCBD-fed mice. The supplementation with SAqFSC-P or PAqFSC-P reduced hepatic total cholesterol levels (by 27 - 46%) in HCBD-fed mice. Supplementation with SAqFSC-P or PAqFSC-P markedly lowered hepatic glucose levels (by 13 - 30%) in ND- and HCBD-fed mice. SAqFSC-P decreased serum alanine aminotransferase (ALT) activity, but PAqFSC-P increased hepatic protein contents in ND-fed mice. Bicylol, as a positive control, reduced ALT activity. In addition, mice supplemented with FSC-P or bicylol showed a smaller body weight gain and adipose tissue mass as compared to the respective un-supplemented ND- or HCBD-fed mice.
The results indicate that SAqFSC-P and PAqFSC-P produce hepatic lipid- and glucose-lowering as well as serum TG-lowering effects in hypercholesterolemic mice. FSC pulp may provide a safe alternative for the management of fatty liver and/or lipid disorders in humans.
Lipids in Health and Disease 03/2014; 13(1):46. · 2.31 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Kinase inhibitors (KIs) represent an important group of anticancer drugs and many of them are substrates and inhibitors of human cytochrome P450s (CYPs), raising the potential of drug interactions. This study investigated the effect of a library of KIs (n = 91) including eleven FDA-approved KIs on human CYP1A2, 2D6, 2C9 and 3A4 using high throughput screening kits and the binding modes with CYPs using the Discovery Studio program 3.1. The KIs exhibited differential inhibitory effect on CYP1A2, 2D6, 2C9 and 3A4, while some of them showed activating effect on CYP2C9 and 3A4. For example, SP 600125 was a potent inhibitor for CYP1A2, but enhanced the activity of CYP2C9 four folds. Among the 80 KIs that are not used clinically, about 13% showed significant inhibition to CYPs. Nilotinib, sunitinib and imatinib were found to be potent CYP1A2 inhibitor. Our docking studies have demonstrated the importance of multiple amino acid residues in the active sites of CYP1A2, 2C9, 2D6, and 3A4 in binding with various KIs. Finally, the in vitro data were used to predict potential KI-drug interactions. These findings indicate that many KIs can serve as CYP inhibitors and further studies are needed to examine the clinical impact. This article is protected by copyright. All rights reserved.
Fundamental and Clinical Pharmacology 02/2014; · 1.99 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Recent studies have been conducted to examine the neuroprotective effects of acupuncture in many neurological disorders. Although the neuroprotective effects of acupuncture has been linked to changes in signaling pathways, accumulating evidence suggest the participation of endogenous biological mediators, such as the neurotrophin (NT) family of proteins, specifically, the brain derived neurotrophic factor (BDNF). Accordingly, acupuncture can inhibit neurodegeneration via expression and activation of BDNF. Moreover, recent studies have reported that acupuncture can increase ATP levels at local stimulated points. We have also demonstrated that acupuncture could activate monocytes and increase the expression of BDNF via the stimulation of ATP. The purpose of this article is to review the recent findings and ongoing studies on the neuroprotective roles of acupuncture and therapeutic implications of acupuncture-induced activation of BDNF and its signaling pathway.
International Journal of Molecular Sciences 01/2014; 15(2):3234-52. · 2.46 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Accumulating evidence suggests that intestinal epithelial barrier dysfunction plays an important role in the pathogenesis of hepatic cirrhosis and its complications such as gastrointestinal injury and hepatic encephalopathy. To date, there is no cure for cirrhosis-associated intestinal mucosal lesion and ulcer. This study aimed to investigate the effect of oxymatrine on intestinal epithelial barrier function and the underlying mechanism in carbon tetrachloride (CCl4)-induced cirrhotic rats. Thirty CCl4-induced cirrhotic rats were randomly divided into treatment group, which received oxymatrine treatment (63 mg/kg), and non-treatment group, which received the same dose of 5% glucose solution (vehicle). The blank group (n = 10 healthy rats) received no treatment. Terminal ileal samples were collected for histopathological examination. The expression level of nuclear factor-κB (NF-κB) p65 in ileal tissue was evaluated by immunohistochemistry. The gene and protein expression levels of tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) in ileal tissues were analyzed by reverse-transcriptase polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Additionally, plasma endotoxin level was determined. In comparison to the blank group, a significant alteration in the morphology of intestinal mucosal villi in the non-treatment group was observed. The intestinal mucosal villi were atrophic, shorter, and fractured, and inflammatory cells were infiltrated into the lamina propria and muscular layer. Besides, serious swell of villi and loose structure of mucous membrane were observed. Oxymatrine reversed the CCl4-induced histological changes and restored intestinal barrier integrity. Moreover, oxymatrine reduced the protein expression level of NF-κB p65, TNF-α, and IL-6, which were elevated in the vehicle-treated group. In addition, the serum endotoxin level was significantly decreased after oxymatrine treatment in CCl4-induced cirrhotic rats. The results indicate that oxymatrine improves intestinal barrier function via NF-κB-mediated signaling pathway and may be used as a new protecting agent for cirrhosis-associated intestinal mucosal damage.
PLoS ONE 01/2014; 9(8):e106082. · 3.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Schisandrin B (Sch B), a dibenzocyclooctadiene compound, is isolated from schisandrae fructus (SF). This study was conducted to compare the time- and dose-response between Sch B- and SF oil (SFO)-induced changes in hepatic and serum parameters in mice.
Drug Design, Development and Therapy 01/2014; 8:1429-39. · 3.49 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Mipu1 (myocardial ischemic preconditioning upregulated protein 1), a novel rat gene recently identified in our lab, was expressed abundantly and predominantly in the brain and heart and upregulated in myocardium during myocardial ischemia/reperfusion in rats. In our previous study we found that Mipu1 was an evolutionarily conserved zinc finger-containing transcription factor. However, whether Mipu1 confers myocardial protection remains unknown. In this study, H9c2 myogenic cells were treated with hydrogen peroxide (H2O2) to simulate oxidative stress during myocardial ischemia-reperfusion injury. The expression of Mipu1 at mRNA and protein levels was detected by RT-PCR and Western blotting analysis. To study the effect of Mipu1 on apoptosis and expression of Fas induced by H2O2, full-length Mipu1 cDNA and Mipu1-RNAi plasmids were transiently transfected into H9c2 myogenic cells, and flow cytometry was used to quantitate the percentage of apoptotic cells. The expression of Fas was analyzed by Western blotting assay. The DNA binding and transcription activities of Mipu1 to the Fas promoter were detected by chromatin immunoprecipitation and luciferase reporter assays. The results showed that exposure of H9c2 myogenic cells to H2O2 resulted in a dose- and time-dependent increase in Mipu1 mRNA and protein levels; Mipu1 over-expression inhibited H2O2-induced apoptosis and upregulation of Fas induced by H2O2 in H9c2 myogenic cells; and knockdown of Mipu1 by RNAi promoted apoptosis and upregulation of Fas induced by H2O2. The chromatin immunoprecipition and reporter assays showed the DNA binding and transcription suppressor activities of Mipu1 to Fas promoter region. These results indicate that Mipu1 protected H9c2 myogenic cells from H2O2-induced apoptosis through inhibiting the expression of Fas.
International Journal of Molecular Sciences 01/2014; 15(10):18206-18220. · 2.46 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Triterpenoids have been used for medicinal purposes in many Asian countries because of their anti-inflammatory, antioxidant, antiproliferative, anticancer, and anticarcinogenic properties. Bardoxolone methyl, the C-28 methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) known as CDDO-Me or RTA 402, is one of the derivatives of synthetic triterpenoids. CDDO-Me has been used for the treatment of chronic kidney disease, cancer (including leukemia and solid tumors), and other diseases. In this review, we will update our knowledge of the clinical pharmacokinetics and pharmacodynamics of CDDO-Me, highlighting its clinical benefits and the underlying mechanisms involved. The role of the Kelch-like erythroid cell-derived protein with CNC homology-associated protein 1 (Keap1)/the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in the therapeutic activities of CDDO-Me will be discussed. CDDO-Me contains α,β-unsaturated carbonyl groups on rings A and C that can generate reversible adducts with the thiol groups of Cys residues in target proteins such as Keap1 and IκB kinase. At low nanomolar concentrations, CDDO-Me protects the cells against oxidative stress via inhibition of reactive oxygen species generation, while CDDO-Me at low micromolar concentrations induces apoptosis by increasing reactive oxygen species and decreasinging intracellular glutathione levels. Through Keap1/Nrf2 and nuclear factor-κB pathways, this agent can modulate the activities of a number of important proteins that regulate inflammation, redox balance, cell proliferation and programmed cell death. In a Phase I trial in cancer patients, CDDO-Me was found to have a slow and saturable oral absorption, a relatively long terminal phase half-life (39 hours at 900 mg/day), nonlinearity (dose-dependent) at high doses (600-1,300 mg/day), and high interpatient variability. As a multifunctional agent, CDDO-Me has improved the renal function in patients with chronic kidney disease associated with type 2 diabetes. CDDO-Me has shown a promising anticancer effect in a Phase I trial. This agent is generally well tolerated, but it may increase adverse cardiovascular events. Presently, it is being further tested for the treatment of patients with chronic kidney disease, cancer, and pulmonary arterial hypertension.
Drug Design, Development and Therapy 01/2014; 8:2075-2088. · 3.49 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: sweet (fruit skin), sour (pulp), bitter/pungent (seed core), and saltiness (all parts), can produce a wide spectrum of biological activities in the body. Here, we investigated the effects of the ethanolic extract of SF pulp, seed, or their combination (namely, EtSF-P, EtSF-S, or EtSF-P/S, resp.; collectively called EtSF) on the metabolism of lipids and glucose in normal diet- (ND-) and hypercholesterolemic diet- (HCLD-) fed mice. Supplementation with EtSF significantly reduced hepatic triglyceride and cholesterol levels by 18-47% in both ND- and HCLD-fed mice. EtSF supplementation reduced serum triglyceride levels (approximately 29%), whereas EtSF-P and EtSF-S/P elevated serum cholesterol (up to 26 and 44%, resp.) in HCLD-fed mice. Treatment with EtSF decreased hepatic glucose levels (by 9-44%) in both ND- and HCLD-fed mice. Supplementation with EtSF-S or EtSF-S/P (at 1 and 3%) increased biliary or fecal TC contents in HCLD-fed mice. However, supplementation with EtSF-S/P at 9% reduced biliary TC levels in HCLD-fed mice. EtSF-P or EtSF-S/P supplementation reduced serum alanine aminotransferase activity in HCLD-fed mice. The findings suggested that supplementation with EtSF lowered lipid and glucose accumulation in the liver and increased fecal cholesterol contents in mice. Dietary supplementation with EtSF-P or EtSF-S/P attenuated liver damage in HCLD-fed mice.
Evidence-based complementary and alternative medicine : eCAM. 01/2014; 2014:472638.
[Show abstract][Hide abstract] ABSTRACT: Seventeen acylides bearing an aryl-tetrazolyl alkyl-substituted side chain were synthesized, starting from clarithromycin, via several reactions including hydrolysis, acetylating, esterification, carbamylation, and Michael addition. The structures of all new compounds were confirmed by (1)H nuclear magnetic resonance spectroscopy, (13)C nuclear magnetic resonance spectroscopy, and mass spectrometry. All these synthesized acylides were evaluated for in vitro antimicrobial activities against gram-positive pathogens (Staphylococcus aureus, Staphylococcus epidermidis) and gram-negative pathogens (Pseudomonas aeruginosa, Escherichia coli), using the broth microdilution method. Results showed that compounds 10e, 10f, 10g, 10 h, 10o have good antibacterial activities.
Drug Design, Development and Therapy 01/2014; 8:1515-25. · 3.49 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: With the avalanche of biological sequences generated in the postgenomic age, molecular science is facing an unprecedented challenge, i.e., how to timely utilize the huge amount of data to benefit human beings. Stimulated by such a challenge, a rapid development has taken place in molecular science, particularly in the areas associated with drug development and biomedicine, both experimental and theoretical. The current thematic issue was launched with the focus on the topic of "Molecular Science for Drug Development and Biomedicine", in hopes to further stimulate more useful techniques and findings from various approaches of molecular science for drug development and biomedicine.[...].
International Journal of Molecular Sciences 01/2014; 15(11):20072-20078. · 2.46 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: In recent years, increasing numbers of people have been choosing herbal medicines or products to improve their health conditions, either alone or in combination with others. Herbs are staging a comeback and herbal "renaissance" occurs all over the world. According to the World Health Organization, 75% of the world's populations are using herbs for basic healthcare needs. Since the dawn of mankind, in fact, the use of herbs/plants has offered an effective medicine for the treatment of illnesses. Moreover, many conventional/pharmaceutical drugs are derived directly from both nature and traditional remedies distributed around the world. Up to now, the practice of herbal medicine entails the use of more than 53,000 species, and a number of these are facing the threat of extinction due to overexploitation. This paper aims to provide a review of the history and status quo of Chinese, Indian, and Arabic herbal medicines in terms of their significant contribution to the health promotion in present-day over-populated and aging societies. Attention will be focused on the depletion of plant resources on earth in meeting the increasing demand for herbs.
Evidence-based complementary and alternative medicine : eCAM. 01/2014; 2014:525340.
[Show abstract][Hide abstract] ABSTRACT: Plumbagin (PLB) has shown anti-cancer activity but the mechanism is unclear. This study has found that PLB has a potent pro-apoptotic and pro-autophagic effect on A549 and H23 cells. PLB arrests cells in G2/M phase, and increases the intracellular level of reactive oxygen species in both cell lines. PLB dose-dependently induces autophagy through inhibition of PI3K/Akt/mTOR pathway as indicated by reduced the phosphorylation of Akt and mTOR. Inhibition or induction of autophagy enhances PLB-induced apoptosis. There is crosstalk between PLB-induced apoptosis and autophagy. These findings indicate that PLB initiates both apoptosis and autophagy in NSCLC cells through coordinated pathways.
[Show abstract][Hide abstract] ABSTRACT: One of the major mechanisms involved in acetaminophen (APAP)-induced hepatotoxicity is the hepatocyte nuclear factor 4α(HNF4α)-mediated activation of pregnane X receptor (PXR) and constitutive androstane receptor (CAR). In the present study, we investigated the role of miR-561 and its target gene DAX-1 encoding a co-repressor of HNF4α in the process of APAP-induced hepatotoxicity. Both HepG2 cells and primary human hepatocytes were used in this study. The levels of reactive oxygen species, lactate dehydrogenase, and glutathione were monitored. Our bioinformatic study suggests an association between miR-561 and DAX-1, but not HNF4α. Treatment of HepG2 cells with APAP caused reduced expression of DAX-1 in a concentration-dependent manner. miR-561 was specifically induced by APAP treatment in HepG2 cells. Transfection of HepG2 cells with a miR-561 mimic resulted in enhanced APAP-induced hepatotoxicity. HNF4αis physically associated with DAX-1 in HepG2 cells. A decreased protein level of DAX-1 by APAP treatment was also enhanced by a miR-561 mimic transfection in HepG2 cells and primary human hepatocytes. The basal and APAP-induced expression of PXR and CAR was enhanced by miR-561 mimic transfection. However, transfection of HepG2 cells with a miR-561 inhibitor or DAX-1 siRNA reversed these effects. Additionally, the chromatin immunoprecipitation assay revealed that recruitment of DAX-1 onto the PXR promoter was inversely related with the recruitment of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α) and HNF4α upon APAP treatment. These results indicate that miR-561 worsens APAP-induced hepatotoxicity probably via inhibition of DAX-1 and consequent increased activation of nuclear receptors.
Drug metabolism and disposition: the biological fate of chemicals 10/2013; · 3.74 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The recurrence and metastatic spread of cancer are major drawbacks in cancer treatment. Although chemotherapy is one of the most effective methods for the treatment of metastatic cancers, it is nonspecific and causes significant toxic damage. The development of drug resistance to chemotherapeutic agents through various mechanisms also limits their therapeutic potential. However, as we discuss here, the use of nanodelivery systems that are a combination of diagnostics and therapeutics (theranostics) is as relatively novel concept in the treatment of cancer. Such systems are likely to improve the therapeutic benefits of encapsulated drugs and can transit to the desired site, maintaining their pharmaceutical properties. The specific targeting of malignant cells using multifunctional nanoparticles exploits theranostics as an improved agent for delivering anticancer drugs and as a new solution for overriding drug resistance.
Drug discovery today 09/2013; · 6.63 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Thiazolidinediones (TZDs) which are synthetic PPARγ agonists are highly effective for treatment of type 2 diabetes. However, the side effect of fluid retention has significantly limited their application. Most of the previous studies addressing TZD-induced fluid retention employed healthy animals. The underlying mechanism of this phenomenon is still incompletely understood, particularly in the setting of disease state. The present study was undertaken to examine rosiglitazone (RGZ)-induced fluid retention in db/db mice and to further investigate the underlying mechanism. In response to RGZ treatment, db/db mice exhibited an accelerated plasma volume expansion as assessed by hematocrit (Hct) and fluorescent nanoparticles, in parallel with a greater increase in body weight, as compared with lean controls. In response to RGZ-induced fluid retention, urinary Na(+) excretion and urine volume were significantly increased in lean mice. In contrast, the natriuretic and diuretic responses were significantly blunted in db/db mice. RGZ db/db mice exhibited a parallel decrease in plasma Na(+) concentration and plasma osmolality, contrasting to unchanged levels in lean controls. Imunoblotting analysis showed downregulation of renal AQP2 expression in response to RGZ treatment in lean mice but not in db/db mice. Renal AQP3 protein expression was unaffected by RGZ treatment in lean mice but was elevated in db/db mice. In contrast, the expression of NHE3 and NKCC2 was unchanged in either mouse strain. Together these results suggest that compared with the lean controls, db/db mice exhibited accelerated plasma volume expansion that was in part due to the inappropriate response of renal water transporters.
[Show abstract][Hide abstract] ABSTRACT: Abstract Despite the advances in science and technology and wide use of chemical drugs, dietary intervention (or food therapy) remains useful in preventing or treating many human diseases. A huge body of evidence shows that the dietary pattern or habit is also an important contributing factor to the development of chronic diseases such as hypertension, type 2 diabetes, hyperlipidemia and cancers. In recent years, over-the-counter health foods, nutraceuticals and plant-derived medicinal products have been gaining popularity all over the world, particularly in developed countries. Unfortunately, owing to the contamination with various harmful substances in foods and the presence of toxic food components, food-borne diseases have also become increasingly problematic. Incidents of food poisonings or tainted food have been increasing worldwide, particular in China and other developing countries. Therefore, the government should put in a greater effort in enforcing food safety by improving the surveillance mechanism and exerting highest standards of quality control for foods.
Critical Reviews in Food Science and Nutrition 08/2013; · 4.82 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: There are no sensitive and specific biomarkers that aid in the clinical diagnosis and prognosis of hepatocellular carcinoma (HCC). The aim of the present study was to determine the mRNA and protein expression levels of beclin 1 (BECN1) and nuclear factor-κB (NF-κB)p65 in patients with HCC, to evaluate their value as potential diagnostic and prognostic biomarkers. Immunohistochemistry and in situ hybridization were used to detect the expression of hepatic BECN1 and NF-kBp65 in patients with HCC, hepatitis B virus (HBV) or cirrhosis, as compared with the expression levels in healthy subjects. The expression level of the BECN1 protein in the HCC tissue was significantly high compared with that in the cirrhotic, hepatitis and normal tissues. The expression of the BECN1 protein in the hepatitis tissue was significantly high compared with that of the cirrhotic and normal tissues. The expression of the BECN1 mRNA in the cancer tissue was significantly high compared with that of the cirrhotic and normal tissues, and the expression of the BECN1 mRNA in the hepatitis tissue was significantly higher than that of the cirrhotic and normal tissues. The expression of the NF-κBp65 protein in the cancer tissue was significantly high compared with that of the cirrhotic, hepatitis and normal tissues. The expression of the NF-κBp65 mRNA in-the cancer tissue was significantly high compared with that of the cirrhotic, hepatitis and normal tissues. BECN1 expression was positively correlated with NF-κBp65 expression in HCC. The abnormal expression of BECN1 and NF-κBp65 was closely associated with the development of HCC. Finally, a search in GeneGo pathway database observed a link between BECN1 and NF-κBp65 through multiple proteins. These results indicate that BECN1 and NF-κBp65 are upregulated in HCC, and that they may serve as useful biomarkers for HCC.