Differences in categorical measures across ordinal groups (i.e., Pexidartinib datasheet educational attainment and iron scores) were assessed using a Jonckeere-Terpstra test, or the exact equivalent. Continuous measures were summarized as medians and interquartile ranges with differences in group distributions assessed using a Wilcoxon rank sum test (for comparison of two groups) or a Kruskal-Wallis test (for comparison

of more than two groups). To assess whether changes in lipid profile measures significantly differed from baseline, a Wilcoxon sign rank test was used. Associations between the proportion of PEG-IFN and ribavirin taken with changes in serum MEK inhibitor lipids were assessed using Spearman’s correlation analyses. For all statistical tests, P < 0.05 was considered statistically significant. To evaluate factors associated with SVR, a relative risk model was employed with a robust variance

estimator.38 In regression models, TG, HDLc, and TC were transformed to the natural logarithm scale to achieve normality. All continuous predictors were centered. The relationships between baseline and 24-week changes during treatment in lipid profile measures and the probability of SVR were graphically assessed using smoothing spline plots. Due to different patterns observed by gender, smoothing spline plots for HDLc were examined separately for males and females. Two types of multivariable models of SVR were constructed using a stepwise approach. One type of multivariable model (models 1 and 2) allowed MCE公司 pretreatment characteristics and the amount of PEG-IFN taken during the first 24 weeks as eligible predictors. Model 2 allowed as additional eligible predictors the baseline lipid profile measures. A second type of multivariable model (model 3) also

adjusted for body weight changes and allowed for the inclusion of variables representing baseline and changes in lipid profile measures during the first 24 weeks of therapy as eligible predictors. To compare the prediction of multivariable models, differences in area under the receiver operating curves (AUROCs) were assessed using a nonparametric method.39 Baseline characteristics of the 330 participants are shown in Table 1. AAs did not significantly differ from CAs by age, gender, employment status, health risk behaviors (smoking status and weekly alcohol consumption), viral level, aspartate aminotransferase, international normalized ratio, white blood cell count, platelet count, percent iron/total iron-binding capacity, Ishak fibrosis, total histological activity index score, steatosis, TG, HDLc, or TC. Compared with CAs, a larger percentage of AAs had health insurance coverage (87% versus 78%, P = 0.

Therefore, HBsAg is not a reliable marker in monitoring the effectiveness of treatment in patients with oral antivirals. Key Word(s): 1.

Hepatitis B; 2. HbsAg; 3. HBV-DNA; 4. Interferon; Presenting Author: KAMRANB. LANKARANI Additional Authors: FARIBORZ GHAFFARPASAND, MOJTABA MAHMOODI, this website MEHRZAD LOTFI, NIMA ZAMIRI, SEYED TAGHI HEYDAR, MOHAMMAD KAZEM FALLAHZADEH, NAJMEH MAHARLOUEI, MEISAM BABAEINEJAD, SOHEILA MEHRAVAR Corresponding Author: KAMRANB. LANKARANI Affiliations: Health Policy Research Center, Shiraz University of Medical Sciences; Health Policy Research Center, Shiraz University of Medical Sciences; Health Policy Research Center, Shiraz University of Medical Sciences; Health Policy Research selleck Center, Shiraz University of Medical Sciences; Health Policy Research Center, Shiraz University of Medical Sciences; Health Policy Research Center, Shiraz University of Medical Sciences; Health Policy Research Center, Shiraz University of Medical Sciences; Health Policy Research Center, Shiraz University of Medical Sciences; Health Policy Research Center, Shiraz University of Medical Sciences Objective: The prevalence and associated

risk factors of NAFLD may vary in different geographical region. Population based studies on prevalence and risk factors of NAFLD in Iranian population are few. The main aim of this population-based study was to determine the prevalence of NAFLD and its risk factors in a sample of adult Iranian population of southern Iran. Methods: This was a cross-sectional study being performed in Shiraz, southern Iran during a 10-month period from November 2010 to September 2011 through cluster random sampling of Iranian general population in Shiraz region. All individuals underwent anthropometric and blood pressure measurements and thorough medical history and physical examinations. Laboratory measurements included fasting blood glucose (FBS), lipid profile, complete blood count (CBC) and liver

function tests. NAFLD was diagnosed by transabdominal ultrasonography. Results: Overall we included 819 subjects in this study among which there were 340 males (41.5%) and 479 females (58.5%) with the mean age of 43.1 ± 14.1 上海皓元 years. NAFLD was diagnosed in 176 (21.5%) subjects. Patients with NAFLD were significantly older (p < 0.001), had higher proportion of male gender (p = 0.004) and had higher BMI (p < 0.001). They also had higher prevalence of hypertension (p < 0.001), high FBS (p < 0.001), high cholesterol (p = 0.026), high triglyceride (p < 0.001) and high waist circumference (p < 0.001). Taking all these together, patients with NAFLD had significantly higher prevalence of metabolic syndrome when compared to healthy subjects (p < 0.001). Conclusion: The prevalence of NAFLD in this group of Iranian adult general population is 21.5%. NAFLD in Iranian population is associated with male gender, old age, obesity, and features of metabolic syndrome. Key Word(s): 1. NAFLD; 2. Prevalence; 3.

No serious complications occurred in either group. Conclusions: 

In this retrospective and small case series, guidewire cannulation after needle-knife fistulotomy increased the success rate of selective bile duct cannulation in patients with difficult bile duct access. “
“Cyclin G1 deficiency is associated with reduced http://www.selleckchem.com/products/LDE225(NVP-LDE225).html incidence of carcinogen-induced hepatocellular carcinoma (HCC), but its function in HCC progression remains obscure. We report a critical role of cyclin G1 in HCC metastasis. Elevated expression of cyclin G1 was detected in HCCs (60.6%), and its expression levels were even higher in portal vein tumor thrombus. Clinicopathological analysis revealed a close correlation of cyclin G1 expression with distant metastasis and poor prognosis of HCC. Forced expression of cyclin G1 promoted epithelial-mesenchymal transition (EMT) and metastasis of HCC cells in vitro and in vivo. Cyclin G1 overexpression enhanced Akt activation through interaction with p85 (regulatory subunit of phosphoinositide 3-kinase [PI3K]), which led to subsequent phosphorylation of glycogen

synthase kinase-3β (GSK-3β) and stabilization of Snail, a critical EMT mediator. Gemcitabine These results suggest that elevated cyclin G1 facilitates HCC metastasis by promoting EMT via PI3K/Akt/GSK-3β/Snail-dependent pathway. Consistently, we have observed a significant correlation between cyclin G1 expression and p-Akt levels in a cohort of HCC patients, and found that combination of these two parameters is a more powerful predictor of poor prognosis. Conclusions: Cyclin G1 plays a pivotal role in HCC metastasis and may serve as a novel prognostic biomarker and therapeutic target. (HEPATOLOGY 2012;55:1787–1798) Cyclin G1 was first

identified serendipitously in screening for Src kinase family in rat fibroblasts.1 It has been categorized as a cyclin on account of possessing a well-conserved cyclin box, although it lacks a destruction box or PEST (Pro, Glu, Ser and Thr)-rich sequences that are responsible for cyclin degradation.1 Cyclin G1 has been well documented as a p53-responsive gene and could be transcriptionally activated by p53 or p73.2, 3 In fact, p53 is the 上海皓元 major factor regulating cyclin G1 expression upon DNA damage.4 Cyclin G1 was reported to interact with the B′ regulatory subunit of protein phosphatase 2A, which in turn dephosphorylated MDM2 followed by p53 degradation.5 A feedback regulation of p53 by cyclin G1 was also observed in cyclin G1-null mouse embryo fibroblasts, which exhibited increased p53 levels.6, 7 Additionally, cyclin G1 was found to interact with certain proteins involved in cell cycle regulation, such as cyclin G–associated kinase and cyclin-dependent kinase 5, but the physiologic significance of these interactions remains elusive.8 Cyclin G1–deficient mice have been reported to be viable without any apparent phenotype.

No serious complications occurred in either group. Conclusions: 

In this retrospective and small case series, guidewire cannulation after needle-knife fistulotomy increased the success rate of selective bile duct cannulation in patients with difficult bile duct access. “
“Cyclin G1 deficiency is associated with reduced Crizotinib incidence of carcinogen-induced hepatocellular carcinoma (HCC), but its function in HCC progression remains obscure. We report a critical role of cyclin G1 in HCC metastasis. Elevated expression of cyclin G1 was detected in HCCs (60.6%), and its expression levels were even higher in portal vein tumor thrombus. Clinicopathological analysis revealed a close correlation of cyclin G1 expression with distant metastasis and poor prognosis of HCC. Forced expression of cyclin G1 promoted epithelial-mesenchymal transition (EMT) and metastasis of HCC cells in vitro and in vivo. Cyclin G1 overexpression enhanced Akt activation through interaction with p85 (regulatory subunit of phosphoinositide 3-kinase [PI3K]), which led to subsequent phosphorylation of glycogen

synthase kinase-3β (GSK-3β) and stabilization of Snail, a critical EMT mediator. Small molecule library These results suggest that elevated cyclin G1 facilitates HCC metastasis by promoting EMT via PI3K/Akt/GSK-3β/Snail-dependent pathway. Consistently, we have observed a significant correlation between cyclin G1 expression and p-Akt levels in a cohort of HCC patients, and found that combination of these two parameters is a more powerful predictor of poor prognosis. Conclusions: Cyclin G1 plays a pivotal role in HCC metastasis and may serve as a novel prognostic biomarker and therapeutic target. (HEPATOLOGY 2012;55:1787–1798) Cyclin G1 was first

identified serendipitously in screening for Src kinase family in rat fibroblasts.1 It has been categorized as a cyclin on account of possessing a well-conserved cyclin box, although it lacks a destruction box or PEST (Pro, Glu, Ser and Thr)-rich sequences that are responsible for cyclin degradation.1 Cyclin G1 has been well documented as a p53-responsive gene and could be transcriptionally activated by p53 or p73.2, 3 In fact, p53 is the 上海皓元医药股份有限公司 major factor regulating cyclin G1 expression upon DNA damage.4 Cyclin G1 was reported to interact with the B′ regulatory subunit of protein phosphatase 2A, which in turn dephosphorylated MDM2 followed by p53 degradation.5 A feedback regulation of p53 by cyclin G1 was also observed in cyclin G1-null mouse embryo fibroblasts, which exhibited increased p53 levels.6, 7 Additionally, cyclin G1 was found to interact with certain proteins involved in cell cycle regulation, such as cyclin G–associated kinase and cyclin-dependent kinase 5, but the physiologic significance of these interactions remains elusive.8 Cyclin G1–deficient mice have been reported to be viable without any apparent phenotype.

4D). Furthermore, EphrinA2-induced activation of NF-κB was blocked by LY294002, NSC23766, dominant-negative Akt, and dominant-negative Rac1, respectively, despite varied inhibitory effects (Fig. 6D). These results indicated that the Rac1/Akt pathway participates in

the modulation of NF-κB activity stimulated by EphrinA2, thus revealing an exquisite regulatory network between EphrinA2, Rac1, Akt, and NF-κB. We identified the relationship between EphrinA2 expression and the development of HCC. The level of EphrinA2 was lowest in normal hepatocytes and increased in primary HCC cells, and it reached the highest level in portal vein tumor thrombus cells. This gradually increasing expression pattern paralleled with deterioration www.selleckchem.com/products/dabrafenib-gsk2118436.html of this disease, suggesting a potential role of EphrinA2 in the progression of HCC. In fact, an emerging body of evidence suggests an increasing role of Eph/Ephrins in cancer. For example, EphA2 can

promote growth of breast, prostate, and pancreas cancer cells, perhaps by activating mitogen-activated protein kinases (MAPKs).7, 8 Likewise, EphA2 and EphB4 can stimulate cancer cell migration and invasion.28 The Eph/Ephrins also can enhance angiogenesis during cancer progression.29, 30 In our study, we demonstrated that EphrinA2 could endow the HCC cells with resistance to both basal and cytokine-induced apoptosis, thus providing a growth advantage to cancer cells, which consequently enhanced the development and progression 上海皓元医药股份有限公司 of HCC. Because the mechanism underlying the regulation of cell survival and apoptosis by Eph/Ephrins in cancer cells remains largely unknown,31 our study provides Autophagy Compound Library novel insights into this mechanism. HCCs are often associated with chronic hepatitis, especially in Asia. TNF-α has been reported to be closely involved in the pathogenesis of chronic liver disease.22, 32, 33 Released by infiltrating lymphocytes,

TNF-α can trigger both pro-survival and pro-apoptosis signaling through the NF-κB pathway and the caspase8 pathway. The cell fate determination mainly depends on the balance between these two pathways. We found that overexpression of EphrinA2 in HCC cells could activate NF-κB, leading to a shift from apoptosis to survival in the circumstance of TNF-α. This may explain how HCC cells tolerate the high level of such potential apoptotic factors. A series of previous studies have suggested that TNF-α is a promising cytokine for cancer therapy34, 35; however, the clinical outcome was disappointing, mainly because of the nonspecific toxicity of this factor at high dose. Efforts have been made to improve its application, such as modification of TNF-α to ameliorate its specificity aiming at tumor tissues.36 Another potential strategy is to increase the sensitivity of cancer cells to TNF-α, which will decrease the effective dose of the cytokine and avoid unexpected systemic toxicity.

Caco2 cells were stimulated with IL-6 for 24 h and 72 h after over-expression or down-regulation miRNA and SOCS3. The levels of chemokines were measured by enzyme linked immunosorbent assay(ELISA). Results: MiRNA-19b expression was decreased, while SOCS3 protein expression was increased in affected area

of colonic mucosa tissue in active CD. There was an inverse correlation between the expression of miR-19b and SOCS3 protein. Bioinformatic prediction showed that SOCS3 was the target gene of miR-19b. Next, we verified that among the targetscan screened miRNAs, only miR-19b expression was significantly lower than the controls. The luciferase reporter assay confirmed that miR-19b directly recognized 3′ UTR of SOCS3. In vitro, knockdown of miR-19b Opaganib cell line increased SOCS3 expression, and over-expression of miR-19b decreased

SOCS3 expression. Furthermore, down-regulation of miR-19b decreased MIP-3αproduction induced by IL-6 modulated by SOCS3. MIP-3αcan induce restitutive Navitoclax migration of intestinal epithelium. So miR-19b may also play a protective role for CD patients, and participate in the repair of intestinal mucosa. Conclusion: MiR-19b plays a critical role in regulating production of chemokines by targeting SOCS3 in colonic epithelial cells. Key Word(s): 1. SOCS3; 2. microRNA-19b; 3. Crohn’s disease; Presenting Author: AMRO SALEM Additional Authors: KHALED SABER, HASSAN ELNAAMEI, AHMED OURFALI Corresponding Author: AMRO SALEM Affiliations: Saudia Arabia; Saudia Arabia; Saudia Arabia; Saudia Arabia Objective: Background : In Isolated terminal ileum

crohn’s disease with no other intestinal or perianal disease surgery is inevitable outcome. Almost 80% of these patients would require surgery at some stage in their disease course.But only 28% will require further surgery if ileo-cecal resection done, there is longer clinical remission, and there is quicker restoration of quality of life. Methods: Methods: 13 patients who had been medchemexpress operated for isolated ileo-cecal crohn’s were reviewed. Data retrieved retrospectively through Chart review, inclusion criteria is isolated terminal ileum crohn’s disease which have been medically man Disease recurrence was defined as symptoms in addition to endoscopic or radiological evidence of disease activity. Severe disease recurrence was defined as a need for repeat resection surgery. Performa will be used to review files and will include demographic data, symptoms before and after surgery, investigations done, medications used and if complications happened, follow up for 2 years, and quality of life post surgery. Results: Results :3 patients had gastrointestinal symptoms recurrence during 2 years of follow up. No patient required repeat resection surgery. Conclusion: Conclusion: Outcomes of isolated ileo-cecal crohn’s resection are excellent with 77% of patients remaining symptoms free. This should be borne in mind when considering biologic treatment.

38 We confirmed our data in cultures of primary human fetal hepatocytes, which are a more amenable in vitro culture system, given the more robust infection levels achieved compared with adult hepatocytes.39 Primary human fetal hepatocytes, transduced with the RFPnls-IPS HCV reporter system,43 were preincubated with different concentrations of mAb16-71. Parallel cultures were treated with an isotype-matched antibody (negative control) or JS81, an antibody that targets CD81 and click here prevents attachment and infection of HCV (positive control). As shown in Fig. 1C, infection of primary fetal hepatocytes by J6/JFH-1 HCVcc was also reduced in a dose-dependent manner. HCV can

spread directly from an infected Huh-7.5 cell to uninfected neighboring cells, with possibly all four HCV entry factors CD81, SR-BI, claudin, and occludin, being involved in this process.32-34 However, by using Huh-7.5 target cells in which CD81 was selectively knocked down (EGFP-IPS/CD81neg), we have recently shown that HCV cell-to-cell

spread can occur independently of CD81.43 We therefore used this cell line to investigate whether mAb16-71 is capable of inhibiting this alternative transmission route. To this end, HCVcc-infected (Jc1) Huh-7.5 cells were cocultured with uninfected EGFP-IPS/CD81neg cells. EGFP-IPS/CD81neg cells have been previously shown to be essentially nonpermissive to cell-free HCV infection.43 Nevertheless, mixing uninfected EGFP-IPS/CD81neg target cells with infected Huh7.5 cells resulted in an infection of 8%-10% of the target cells. However, in the presence Ibrutinib concentration of increasing concentrations of mAb16-71 a dose-dependent reduction in EGFP-IPS/CD81neg target cell infection was observed, whereas no significant changes

in HCV transmission were observed in the presence of an isotype-matched control antibody (Fig. 1D). This clearly proves that mAb16-71 not only prevents cell-free HCV infection, but also interferes 上海皓元医药股份有限公司 with the direct cell-to-cell transmission route. Given the encouraging results in cell culture, we investigated whether administration of mAb16-71 to “human liver urokinase-type plasminogen activator, severe combined immune deficiency (uPA-SCID)” mice (chimeric mice) could protect these animals from a subsequent challenge with serum-derived virus. These mice have a humanized liver (up to 90% chimerism) and are in addition to the chimpanzee the preferred animal model for reproducible infection with natural HCV isolates.40, 42, 45, 46 Two chimeric mice underwent a 2-week therapy consisting of five intraperitoneal injections, each containing 400 μg of mAb16-71. One day after the first injection, both chimeric mice were challenged with a 100% mouse infectious dose (MID100) of serum-derived genotype 1a HCV (mH77C). In contrast to nontreated control animals, which experienced a rapid increase of viral RNA in their plasma, HCV RNA remained undetectable (<375 IU/mL) in both treated mice in the 12-week observation period (Fig. 2A).

98. It has good construct validity, with a good correlation with other self-rated assessment tools, including the HAL. The FISH had a good correlation with the clinical score (r = –0.61) and the radiological score (r = –0.38) [17]. The FISH was originally designed to compare a patient’s basic functional ability with that of normal healthy individuals, and was not designed to assess challenging activities in individuals. Therefore, like the PedHAL, it may have a ceiling effect when applied to those with minimal

musculoskeletal changes [19]. It has, however, been used effectively in studies from varied cultural backgrounds [20–23]. While the assessment of Activities involves the ability to execute tasks or actions, Participation is defined as involvement in a life situation, such as sport, leisure, Palbociclib cost work or social events [4]. The ICF provides a single list of activities and participation in nine domains. According

to their needs and purposes, investigators designate some domains as activities and others as participation [4]. Although there are several generic instruments used to assess BGB324 concentration participation, only a few have been used in haemophilia [2]. While the items in FISH are primarily in the domain of ‘activities’, the HAL has several questions that involve the subject’s interaction with others and with the environment. Assessing ‘participation’ across cultures is challenging, as several items/questions may not be equally relevant. In a study from India several items related to participation in the HAL had poor cross-cultural validation [17]. The Canadian Occupational Performance Measure (COPM) is an open-ended questionnaire that allows patients to prioritize

their main concerns – both in the domains of functional activities and in participation. It has been shown to be useful in making individualized management plans for patients with haemophilia [24]. Its ability to assess different intervention programmes is, however, limited. The feasibility of developing a tool to assess participation, which is contextually relevant and universally applicable, needs to be explored. It has been a long felt need to develop a core set of disease-specific tools to assess the different domains of musculoskeletal outcome as defined by the ICF. The WFH has taken the first step by identifying a core set of tools, MCE and making them available on the World Wide Web (http://www.wfh.org/2/7/7_0_Compendium_Assessment_Tools.htm). These tools need to be used more widely in centres not involved in their development, to judge their acceptability across different countries. Long-term studies are necessary to determine their efficacy in assessing the severity of joint arthropathy. Radiological assessment has been one of the oldest clinimetric tools used to measure progression of joint arthropathy. With newer imaging modalities, it has been possible to detect changes in joints before they are clinically apparent.

New management options such as prophylaxis have been introduced and new treatment choices in the form of longer acting factor concentrates are on the horizon. In the current clinical environment, inhibitor formation continues to be a major complication in the treatment of patients with haemophilia. Prevention and eradication have therefore become a major focus of clinical and scientific investigation. This supplement is based on an international haemophilia meeting held on 21 September 2013 in Barcelona, Spain, and sponsored by Grifols

S.A. The meeting brought together leading haemophilia and bleeding disorder experts from around the world to discuss advances in BTK inhibitor datasheet inhibitor prevention and optimization of immune tolerance induction (ITI) therapy in patients with haemophilia learn more A and inhibitors. The meeting consisted of three main sessions: The first session featured novel investigations which reinforce the protective role of factor VIII (FVIII)/von Willebrand factor complex in inhibitor development, with presentations by P.M. Mannucci (Milan, Italy), Q. Shi (Milwaukee, WI, USA), S. Bonanad (Valencia, Spain) and R. Klamroth (Berlin, Germany). The second session covered choice of ITI therapy for optimal management of inhibitor patients from both a clinical and pharmacoeconomic perspective, and featured discussions by J.

Oldenburg (Bonn, Germany), S. Austin (London, UK), and C. Kessler (Washington DC, USA). In the final session of the meeting, new predictive approaches for ITI management were discussed by G. Di Minno (Naples, Italy), E. Santagostino (Milan, Italy), K. Pratt (Bethesda, MD, USA) and C. Königs MCE (Frankfurt, Germany). These latter two contributors

presented novel investigators that assist in understanding the immunological response in ITI, a topic that has gained significance in recent years and an area that is anticipated to provide the basis for more targeted and individualized therapy in the future. The author received an honorarium from Grifols S.A. for participating in the international meeting and production of the article. The author thanks Content Ed Net for providing editorial assistance in the preparation of the article, with funding from Grifols S.A. “
“Measurement of the activity of factor VIII (FVIII:C) is a central component of haemophilia care and is used in the diagnosis of and monitoring following treatment with clotting factor concentrate or desmopressin. Although three different assays (the one and two stage clotting and chromogenic assays) have been available for many years, in practice the one-stage clotting assay predominates worldwide. The dominance of the one-stage assay is the result of the international drive for simplicity, automation and cost control.

Results indicated that stable overexpression of the miR-216a/217 cluster significantly promoted the migration ability of HepG2-miR-216a/217 and PLC/PRF/5-miR-216a/217 cells in vitro (Fig. 2E). These data indicated that overexpression of miR-216a/217 in

HCC with epithelial phenotypes induced EMT and enhanced migration abilities. Next, HLE cells with a mesenchymal phenotype were used as recipient cells for transfection of antagomir-miR-216a/217 (Genepharma, Shanghai, China). (Antagomirs, also known as anti-miRs or blockmirs, are a novel class of chemically engineered oligonucleotides used to silence endogenous miRNAs.) After the silencing of miR-216a/217 (Supporting Fig. 3A), striking morphological changes consistent with those of mesenchymal-to-epithelial transition (MET) were observed (Supporting Fig. 3B). Up-regulation of E-cadherin, an epithelial biomarker, and reduced expression of vimentin, a mesenchymal biomarker, JQ1 were also observed (Supporting Fig. 3C). Furthermore, we also PLX4032 mw examined the expression of miR-216a/217 on the proliferation and apoptosis of liver cancer cells. A significant increase in

cell proliferation was observed in PLC/PRF/5 at 72 hours after transfection of the p-miR-216a/217-overexpressing vector, whereas transfection of the antagomir-miR-216a/217 into HLE cells significantly decreased cell proliferation (Supporting Fig. 4A). The number of apoptotic cells (Annexin V+ cells) was not significantly affected in PLC/PRF/5 and HLE cells by modulating expression of the miR-216a/217 cluster (Supporting Fig. 4B). The recent discovery of the emergence of CSCs occurred, in part, as a result of miRNA-mediated EMT, which has provided a new avenue in understanding the regulatory mechanisms in CSCs and drug resistance. Because specific CSC markers have not been well defined for most CSCs, sphere-forming ability has emerged as a useful tool to evaluate the stemness characteristics of cells and for the

enhanced enrichment MCE公司 of potential CSCs. Therefore, we evaluated HepG2-miR-216a/217 and PLC/PRF/5-miR-216a/217 cells for their ability to form tumor spheres. It was observed that HepG2-miR-216a/217 and PLC/PRF/5-miR-216a/217 generated 2∼3-fold more spheres than corresponding control cells (Fig. 3A,B). Flow cytometric analysis further demonstrated that sphere-forming cells derived from HepG2-miR-216a/217 and PLC/PRF/5-miR-216a/217 cells gave an enriched epithelial cell adhesion molecule (EpCAM)+ cell subpopulation, consistent with reported characteristics of liver CSCs[15] (Fig. 3C,D). The parental HepG2 had a small percentage of EpCAM+ cell subpopulation (12.6%), which was increased to 23.9% after transfection with miR-216a/217 (Fig. 3C). This suggests that the miR-216a/217 cluster may play an important role in regulating the stem-like traits of HCC cells by inducing EMT.