Use of AA donors allows consideration of older donors. (Hepatology 2013;58:1263–1269) Hepatitis C virus (HCV) is the leading indication for liver transplantation (LT) in the United States.[1] Compared to Caucasians, African-Americans (AA) have relatively superior outcomes with chronic HCV disease

prior to transplantation,[2, 3] but experience more aggressive recurrence of HCV disease after liver replacement.[4, 5] The 2-year and 5-year graft survival for HCV-positive AA LT recipients has been reported to be as much as 10% lower than in non-AA recipients.[6, 7] The reason for this disparity in outcome is poorly understood. A lower likelihood of responding to antiviral therapy post-LT may be one factor.[8, 9] Donor factors are likely to be of importance NVP-BKM120 also. The Donor Risk Index (DRI)—derived from 20,023 predominantly pre-Model for Endstage Liver Disease (MELD) era U.S. liver transplants—was originally proposed in 2006 to predict LT recipient outcome based on available donor factors. Containing seven donor variables, DRI predicts post-LT graft failure using a continuous, numerical scoring system.[10] The DRI was a milestone in highlighting the importance of donor quality on LT outcomes, and while the inclusion of a large, heterogeneous recipient pool maximized its generalizability, the DRI may have more limited prediction among specific find more subgroups, such as those

transplanted for HCV. Prior retrospective studies have shown a strong and consistent association between donor age and severity of HCV recurrence.[11, 12] Interestingly, in the original DRI, allografts from AA donors, compared to Caucasian donors, were associated with an medchemexpress increased risk (hazard ratio [HR] 1.19, 95% confidence interval [CI] 1.10-1.29, P < 0.001) of posttransplant graft failure (death or re-LT); but several recent studies of HCV-infected transplant recipients have independently demonstrated a trend of improved graft outcomes when AA donor livers were paired with HCV-positive AA recipients.[4, 13, 14] With these observations in mind, we sought to define the donor factors of importance in AA recipients with HCV and to develop a donor

risk model that accurately estimates risk of graft loss for this patient subgroup. With Institutional Review Board (IRB) approval, we examined adult AA recipients of deceased donor liver transplants from March 1, 2002 to December 31, 2009 (MELD-era) with primary, secondary, or other diagnosis of HCV recorded in the UNOS Standard Transplant Analysis and Research (STAR) file created on June 30, 2011. We excluded liver retransplants and recipients with Status 1, human immunodeficiency virus (HIV-coinfection, or less than 30 days of follow-up. The primary outcome was post-LT graft loss (recipient death or retransplant). Recipient and donor factors were described with frequency distributions and medians (interquartile ranges [IQRs]).

Use of AA donors allows consideration of older donors. (Hepatology 2013;58:1263–1269) Hepatitis C virus (HCV) is the leading indication for liver transplantation (LT) in the United States.[1] Compared to Caucasians, African-Americans (AA) have relatively superior outcomes with chronic HCV disease

prior to transplantation,[2, 3] but experience more aggressive recurrence of HCV disease after liver replacement.[4, 5] The 2-year and 5-year graft survival for HCV-positive AA LT recipients has been reported to be as much as 10% lower than in non-AA recipients.[6, 7] The reason for this disparity in outcome is poorly understood. A lower likelihood of responding to antiviral therapy post-LT may be one factor.[8, 9] Donor factors are likely to be of importance INCB018424 nmr also. The Donor Risk Index (DRI)—derived from 20,023 predominantly pre-Model for Endstage Liver Disease (MELD) era U.S. liver transplants—was originally proposed in 2006 to predict LT recipient outcome based on available donor factors. Containing seven donor variables, DRI predicts post-LT graft failure using a continuous, numerical scoring system.[10] The DRI was a milestone in highlighting the importance of donor quality on LT outcomes, and while the inclusion of a large, heterogeneous recipient pool maximized its generalizability, the DRI may have more limited prediction among specific MG-132 subgroups, such as those

transplanted for HCV. Prior retrospective studies have shown a strong and consistent association between donor age and severity of HCV recurrence.[11, 12] Interestingly, in the original DRI, allografts from AA donors, compared to Caucasian donors, were associated with an MCE increased risk (hazard ratio [HR] 1.19, 95% confidence interval [CI] 1.10-1.29, P < 0.001) of posttransplant graft failure (death or re-LT); but several recent studies of HCV-infected transplant recipients have independently demonstrated a trend of improved graft outcomes when AA donor livers were paired with HCV-positive AA recipients.[4, 13, 14] With these observations in mind, we sought to define the donor factors of importance in AA recipients with HCV and to develop a donor

risk model that accurately estimates risk of graft loss for this patient subgroup. With Institutional Review Board (IRB) approval, we examined adult AA recipients of deceased donor liver transplants from March 1, 2002 to December 31, 2009 (MELD-era) with primary, secondary, or other diagnosis of HCV recorded in the UNOS Standard Transplant Analysis and Research (STAR) file created on June 30, 2011. We excluded liver retransplants and recipients with Status 1, human immunodeficiency virus (HIV-coinfection, or less than 30 days of follow-up. The primary outcome was post-LT graft loss (recipient death or retransplant). Recipient and donor factors were described with frequency distributions and medians (interquartile ranges [IQRs]).

Disclosures: The following people have nothing to disclose: Mingyue

Zhu, Junli Guo, Hua Xia, Xieju Xie, Mengsen Li Fibroblast growth factor 4 (FGFR4), a receptor tyrosine kinase, is active and overexpressed in many cancers including cholan-giocarcinoma. We have confirmed expression of FGFR4 and its ligand, fibroblast growth factor 19 (FGF19), in a panel of cholangiocarcinoma cells. Our preliminary studies have identified this signaling pathway as pro-proliferative and anti-apop-totic, and inhibition of FGFR signaling (with click here a small molecule inhibitor, PD173074) decreases proliferation and sensitizes cells to TRAIL-induced apoptosis. Treatment of cholangiocarci-noma cells with FGF19 leads to an increase in FGFR4 levels as well as cleavage of a novel R4-ICD (receptor 4 – intracellular domain), which is lost with FGFR inhibition. We have also identified cell cycle regulation of FGFR4, including R4-ICD. Upon release from G1 block, synchronized cells express higher

levels FGFR4 and R4-ICD at 4 and 8 hours after re-entry into the cell cycle, corresponding to S-phase. In addition, cells treated with PD173074 show cell cycle arrest at G0/G1, and have slower progression through the cell cycle than vehicle treated cells; indicating that FGFR4 is regulated by the cell cycle and can modulate progression through the cell cycle. To begin to evaluate the role of FGFR4 in the cell cycle, we visualized FGFR4 during different cell phases. During G0/G1 and S-phase, FGFR4 is localized Luminespib to the plasma membrane and cytoplasm. In mitotic cells, FGFR4 is decreased

at the plasma membrane and cytoplasm, and is localized at the mitotic spindles. Co-staining with alpha-tubulin and FGFR4 indicates co-localization at the mitotic spindle during mitosis and 上海皓元 at the mid-body during cytokinesis. Preliminary pre-clinical studies in a rat model of cholangiocarcinoma show ∼55% reduction in tumor weight when FGFR signaling is inhibited. Increased cell death was confirmed in tumors exposed to the FGFR inhibitor via TUNEL assay. We are currently evaluating how FGFR4 is cleaved and its role in mitosis at the mitotic spindle. We conclude that FGFR4 signaling is a pro-survival mechanism in cholangiocar-cinoma and have identified a novel function of FGFR4 in cell cycle regulation. Disclosures: The following people have nothing to disclose: Ashley M. Mohr, Mary A. Smith, Sathish Kumar Natarajan, Cody J. Wehrkamp, Carol A. Casey, Justin L. Mott “
“I was flattered when Keith Lindor asked me to contribute to the “Master’s Perspective” series, especially when I saw the list of prior contributors, a “Who’s-Who” of hepatology. It was reassuring that I was friends with all the prior contributors, collaborated with many of them, and was critically mentored by one of them (Alan Hofmann) (Fig. 1A).

However, in Phase 2 trials subjects with detectable/BLOQ HCV RNA at the current RGT decision points (week 8 for boceprevir, week 4 for telaprevir) generally achieved a higher SVR rate and lower relapse rate with an extended duration of treatment. Based on the totality of data presented here, clinicians prescribing boceprevir or telaprevir are cautioned not to consider detectable/BLOQ HCV RNA equivalent to undetectable HCV RNA for the purpose of shortening treatment duration. Ponatinib molecular weight Product inserts for both boceprevir and telaprevir state that for the purpose of assessing RGT eligibility, “a confirmed ‘detectable but below limit of quantification’

HCV-RNA result should not be considered equivalent to an ‘undetectable’ HCV-RNA result.”12, 13 Using a nonvalidated,

making with boceprevir- or telaprevir-based regimens could result in suboptimal SVR rates and elevated relapse rates. In addition, our analyses of the treatment-free follow-up period for SVR-achieving Hydroxychloroquine subjects demonstrated there can be variability in the rate at which detectable/BLOQ results are reported by different contract laboratories using the same HCV RNA assay. Vendor B reported an unexpectedly high rate of detectable HCV RNA results during follow-up among SVR-achieving subjects for telaprevir Study 108, which we hypothesize represents a higher rate of false-positive HCV RNA detection throughout the conduct of the trial. In fact, reanalysis of a subset of Study 108 samples by Vendor A yielded a reduced frequency of detectable/BLOQ results, particularly for follow-up samples from MCE公司 subjects who achieved SVR. Furthermore, the rate at which such follow-up results

were reported by Vendor A for the P05216 and C216 trials is comparable to the recognized false-positive detection rate of the assay: ≈1.3%, according to the FDA-approved assay package insert.17 A higher rate of reported detectable/BLOQ results during treatment and follow-up by Vendor B could explain the decreased difference in SVR rates between subjects with on-treatment detectable/BLOQ versus undetectable HCV RNA levels relative to that observed for the P05216 and C216 trials. However, despite the unexpectedly high rate of detectable/BLOQ results during and following treatment in Study 108, SVR rates remained consistently higher for subjects with undetectable HCV RNA at any given timepoint during treatment compared with those with detectable/BLOQ at the same timepoint. Currently, it is not clear why the detectable/BLOQ reporting frequency varied by contract laboratory, whether such variability still exists, and whether it extends across other laboratories that typically conduct HCV RNA assessments. We cannot confirm the same technical procedures were used by the different laboratories for the Roche COBAS TaqMan HCV 2.0 assay used in the clinical trials.

However, in Phase 2 trials subjects with detectable/BLOQ HCV RNA at the current RGT decision points (week 8 for boceprevir, week 4 for telaprevir) generally achieved a higher SVR rate and lower relapse rate with an extended duration of treatment. Based on the totality of data presented here, clinicians prescribing boceprevir or telaprevir are cautioned not to consider detectable/BLOQ HCV RNA equivalent to undetectable HCV RNA for the purpose of shortening treatment duration. Metformin solubility dmso Product inserts for both boceprevir and telaprevir state that for the purpose of assessing RGT eligibility, “a confirmed ‘detectable but below limit of quantification’

HCV-RNA result should not be considered equivalent to an ‘undetectable’ HCV-RNA result.”12, 13 Using a nonvalidated,

making with boceprevir- or telaprevir-based regimens could result in suboptimal SVR rates and elevated relapse rates. In addition, our analyses of the treatment-free follow-up period for SVR-achieving buy CH5424802 subjects demonstrated there can be variability in the rate at which detectable/BLOQ results are reported by different contract laboratories using the same HCV RNA assay. Vendor B reported an unexpectedly high rate of detectable HCV RNA results during follow-up among SVR-achieving subjects for telaprevir Study 108, which we hypothesize represents a higher rate of false-positive HCV RNA detection throughout the conduct of the trial. In fact, reanalysis of a subset of Study 108 samples by Vendor A yielded a reduced frequency of detectable/BLOQ results, particularly for follow-up samples from 上海皓元医药股份有限公司 subjects who achieved SVR. Furthermore, the rate at which such follow-up results

were reported by Vendor A for the P05216 and C216 trials is comparable to the recognized false-positive detection rate of the assay: ≈1.3%, according to the FDA-approved assay package insert.17 A higher rate of reported detectable/BLOQ results during treatment and follow-up by Vendor B could explain the decreased difference in SVR rates between subjects with on-treatment detectable/BLOQ versus undetectable HCV RNA levels relative to that observed for the P05216 and C216 trials. However, despite the unexpectedly high rate of detectable/BLOQ results during and following treatment in Study 108, SVR rates remained consistently higher for subjects with undetectable HCV RNA at any given timepoint during treatment compared with those with detectable/BLOQ at the same timepoint. Currently, it is not clear why the detectable/BLOQ reporting frequency varied by contract laboratory, whether such variability still exists, and whether it extends across other laboratories that typically conduct HCV RNA assessments. We cannot confirm the same technical procedures were used by the different laboratories for the Roche COBAS TaqMan HCV 2.0 assay used in the clinical trials.

Persian buck groans were relatively long, pulsed calls of almost 1-s duration, with low fundamental frequencies, and relatively weak formant modulation. European buck groans were much shorter (0.38 s), but with similarly low fundamental frequencies and

clearer formant modulation. We found some minor differences in the formant frequencies (F4 and F5) of calls of the two European fallow populations. Given the length of time since Persian and European fallow deer diverged, and that both their mitochondrial and nuclear genomes are very different, it is notable that the structure of their groans is Barasertib purchase still so similar. Our findings suggest that the factors influencing the evolution of these vocalizations (e.g. sensory system characteristics, environment and mate choice) have probably been similar

for both species. Vocal communication is used to regulate social interactions, including those linked to sexual selection (Andersson, 1994). The sexually selected calls of males function in attracting mates and repelling competitors (Reby & McComb, 2003a; Briefer, Vannoni & McElligott, 2010; Koren & Geffen, 2011). The source–filter theory of call production has become the standard approach for examining the acoustic parameters of mammal vocalizations. It is advantageous because it links an animal’s morphology and physiology, to its vocal parameters (Taylor & Reby, 2010; hypoxia-inducible factor cancer Briefer & McElligott, 2011). Call structure in mammals results from a two-stage source–filter process linked to the larynx and vocal tract (Taylor & Reby, 2010). The 上海皓元医药股份有限公司 air expelled from the lungs causes vibrations of the vocal folds in the larynx, and generates the glottal wave (‘source’). The rate of these vibrations determines the fundamental frequency (F0, Taylor & Reby, 2010). The sound then passes through the supralaryngeal vocal tract and nasal cavities and gets filtered. This filtering determines the vocal tract resonances or formant frequencies (Taylor & Reby, 2010; Briefer & McElligott, 2011). The sound that finally emanates

from an animal results from this source–filter process. Body size is also linked to lung capacity, which is an important determinant of call duration (Fitch, 2006). Using the source–filter approach when examining the calls of a species that has not been previously studied, allows direct and detailed comparisons with more well-known ones (Cap et al., 2008; Kidjo et al., 2008; Frey & Riede, 2013). The fallow deer genus Dama diverged from the Cervinae, and later split into two species during the Pliocene epoch; between 4.13 and 2.85 MYA (Persian fallow deer Dama mesopotamica and European fallow deer Dama dama; Gilbert, Ropiquet & Hassanin, 2006; Hassanin et al., 2012). Until recently, questions remained about whether the two types were distinct enough to be considered species or subspecies (Fernández-García, 2012).

Administered dosages were tapered towards a normal prophylactic regimen of 15–25 IU

FVIII kg−1 three times a week, according to previously described intermediate dose prophylaxis [11]. When FVIII treatment was started because of a life threatening bleed or surgery, and the inhibitor level was less than 10 BU mL, an initial bolus with FVIII was given to neutralize the inhibitor [4], followed by 25 IU kg−1 FVIII twice daily for Dorsomorphin supplier 1–2 weeks, depending on the clinical status of the patient and the anamnestic response to FVIII. During ITI in patients with a high titre inhibitor, surgical procedures, such as insertion of a PAC system, were covered with recombinant factor VIIa (rVIIa, Novoseven®; NovoNordisk, Copenhagen, Denmark). Bleeds were treated with both APCC (Feiba®; Baxter, Vienna, MI-503 in vivo Austria) or rVIIa (Novoseven®). Plasma sampling  Plasma samples to determine FVIII levels

and inhibitor assays were collected using standard techniques: 4.5 mL venous blood was drawn in a vacutainer in which 0.5 mL sodium citrate (109 mol L−1) was added as an anticoagulant. After centrifugation at 3000 × g for 15 min at 4°C, the platelet-poor plasma was carefully pipetted off and plasma was stored at −20°C. In small children 1 mL cups were used, containing 0.1 mL sodium citrate to which 0.9 mL blood was added. Inhibitor assays  Factor VIII antibodies were initially performed according to the Bethesda MCE公司 method as described by Kasper et al. [12]. In 1995, the Nijmegen modification was introduced [13]. This modification was subsequently used in our laboratory. Antibody titres of ≥1 BU mL−1 were defined as positive in the original test, whereas antibody titres >0.3 BU mL−1 were considered positive in the Nijmegen modification. With exception of patient one, all samples tested with the original Bethesda assay were retested with the Nijmegen assay. For this study, only the results of the Nijmegen assay were used. Inhibitor patients were tested every 4–8 weeks during their ITI treatment and the first 6 months

after successful ITI. Subsequently inhibitor tests were carried out once or twice yearly until end of follow-up. Factor VIII assay  Factor VIII assays were performed using the one stage method and expressed as a percentage of FVIII present in normal pooled human plasma. In vivo recovery and factor VIII half life  To determine in vivo recovery in patients with an inhibitor titre below 10 BU mL−1, blood samples were taken before, and 15–30 min after FVIII infusion. Recovery was defined as the level of FVIII measured in relation to the expected level of FVIII, calculated according to Lee et al. [14]. A FVIII recovery of 66% or more was considered normal. Factor VIII half life was determined after a wash out period of 72 h.

No quantitative syntheses of these studies have been performed. A systematic review and meta-analysis were conducted to examine the prevalence of inherited AT, PC,

and PS deficiencies in these patients and to compare the prevalence with healthy subjects. PubMed, EMBASE, and Cochrane Library databases were employed to identify all studies in which inherited AT, PC, and PS deficiencies in PVST and/or BCS were evaluated by family study or gene analysis. Prevalence and odds ratios of these inherited deficiencies were pooled; heterogeneity Selleck Small molecule library among studies was evaluated. Nine studies were included in our meta-analysis. The pooled prevalence of inherited AT, PC, and PS deficiencies were 3.9%, 5.6%, and 2.6% in PVST, and 2.3%, 3.8%, and 3.0% in BCS, respectively. Heterogeneity among studies was not significant except for the analysis of inherited PC deficiency in BCS. Three studies compared the prevalence TSA HDAC purchase of these inherited deficiencies between PVST patients and

healthy subjects. The pooled odds ratios of inherited AT, PC, and PS deficiencies for PVST patients were 8.89 (95% confidence interval [CI] 2.34–33.72, P = 0.0011), 17.63 (95% CI 1.97–158.21, P = 0.0032), and 8.00 (95% CI 1.61–39.86, P = 0.011), respectively. Only one study demonstrated that no inherited deficiency was found in both BCS patients and healthy subjects. Inherited AT, PC, and PS deficiencies are rare in PVST and BCS. These inherited deficiencies

increase the risk of PVST. “
“To the Editor: We enjoyed the well-written review by Ratziu et al.1 on the role of insulin sensitizers in nonalcoholic steatohepatitis (NASH). However, we would like to correct two minor errors regarding our study2 and share our ongoing efforts that address some of the knowledge gaps highlighted by the authors. Table 1 in Ratziu et al.’s review states that we recruited only patients with diabetes. As reported elsewhere,3, 4 this is incorrect. We designed the study in 2002, and within the context of the emerging liver toxicity associated with troglitazone, we felt that exposure to a thiazolidinedione (TZD) should be reserved for NASH patients with type 2 diabetes mellitus (T2DM), or nondiabetic patients at risk of developing T2DM (i.e., impaired glucose tolerance [IGT]), so that the risk/benefit ratio 上海皓元 of treatment would favor patients at least by improving glucose metabolism (the progression from IGT to T2DM is ≈6%-10% per year). Therefore, at study entry, patients were screened with an oral glucose tolerance test. Only 14% of all patients screened (n = 70) had known T2DM. Among those patients believed to have normal glucose metabolism (n = 60), 49% had IGT, and 30% were diagnosed with new-onset T2DM, whereas only 21% had normal glucose metabolism (the latter patients were excluded from the study). These results are similar to more recent work by our group.

No quantitative syntheses of these studies have been performed. A systematic review and meta-analysis were conducted to examine the prevalence of inherited AT, PC,

and PS deficiencies in these patients and to compare the prevalence with healthy subjects. PubMed, EMBASE, and Cochrane Library databases were employed to identify all studies in which inherited AT, PC, and PS deficiencies in PVST and/or BCS were evaluated by family study or gene analysis. Prevalence and odds ratios of these inherited deficiencies were pooled; heterogeneity www.selleckchem.com/products/cobimetinib-gdc-0973-rg7420.html among studies was evaluated. Nine studies were included in our meta-analysis. The pooled prevalence of inherited AT, PC, and PS deficiencies were 3.9%, 5.6%, and 2.6% in PVST, and 2.3%, 3.8%, and 3.0% in BCS, respectively. Heterogeneity among studies was not significant except for the analysis of inherited PC deficiency in BCS. Three studies compared the prevalence Rapamycin of these inherited deficiencies between PVST patients and

healthy subjects. The pooled odds ratios of inherited AT, PC, and PS deficiencies for PVST patients were 8.89 (95% confidence interval [CI] 2.34–33.72, P = 0.0011), 17.63 (95% CI 1.97–158.21, P = 0.0032), and 8.00 (95% CI 1.61–39.86, P = 0.011), respectively. Only one study demonstrated that no inherited deficiency was found in both BCS patients and healthy subjects. Inherited AT, PC, and PS deficiencies are rare in PVST and BCS. These inherited deficiencies

increase the risk of PVST. “
“To the Editor: We enjoyed the well-written review by Ratziu et al.1 on the role of insulin sensitizers in nonalcoholic steatohepatitis (NASH). However, we would like to correct two minor errors regarding our study2 and share our ongoing efforts that address some of the knowledge gaps highlighted by the authors. Table 1 in Ratziu et al.’s review states that we recruited only patients with diabetes. As reported elsewhere,3, 4 this is incorrect. We designed the study in 2002, and within the context of the emerging liver toxicity associated with troglitazone, we felt that exposure to a thiazolidinedione (TZD) should be reserved for NASH patients with type 2 diabetes mellitus (T2DM), or nondiabetic patients at risk of developing T2DM (i.e., impaired glucose tolerance [IGT]), so that the risk/benefit ratio MCE of treatment would favor patients at least by improving glucose metabolism (the progression from IGT to T2DM is ≈6%-10% per year). Therefore, at study entry, patients were screened with an oral glucose tolerance test. Only 14% of all patients screened (n = 70) had known T2DM. Among those patients believed to have normal glucose metabolism (n = 60), 49% had IGT, and 30% were diagnosed with new-onset T2DM, whereas only 21% had normal glucose metabolism (the latter patients were excluded from the study). These results are similar to more recent work by our group.

HE staining was used to observe the distribution of CIK and tumor cells. Further, antitumor activity of CIK cells was examined in nude mouse xenograft model. Ten nude mice were injected with 6 × 106 TE3 cells subcutaneously. Five days later, CIK cells (5 × 107) (experiment group) or BPS (control group) was injected into nude mice intravenously once a week. Results: The CIK cell population contained 97.39% CD3+ cells and 39.8% CD3+CD56+ cells. At the effector-target cell ratio of 30:1, CIK cells killed nearly 50% of TE3 cells. HE staining showed CIK cells aggregated around TE3 cells when they were co-cultured. In nude mice model,

tumor weight was reduced in CIK cells LDE225 cell line treated group compared with control group (0.21 ± 0.07 g vs. 0.53 ± 0.10 g, P < 0.05). Here, we provide evidences that CIK cells had an growth inhibition effect on esophageal squamous cells carcinoma in vitro and in vivio. Conclusion: CIK cells therapy may be a candidate choice for esophageal cancer patients. Key Word(s): 1. esophageal cancer; 2. immunotherapy; 3. CIK cells; Presenting

Author: LINLIN REN Additional Authors: JIE HONG, JINGYUAN FANG Corresponding Author: JIE HONG, JINGYUAN FANG Affiliations: Renji Hospital, Shanghai Jiao-Tong University School of Medicine Objective: The polycomb group protein EZH2, which has histone methyltrasferase (HMT) activity, has been increasingly studied recently. It was reported that EZH2 is involved in many processes www.selleckchem.com/products/Bortezomib.html such as cell cycle, apoptosis. However, whether EZH2 participates in the process of authphagy and its regulatory mechanism in CRC (colorectal cancer) remains unclear. Methods: ZEB1, EZH2 and PTEN expression were measured by Western Blot and immunohistochemistry respectively. ZEB1, EZH2 and PTEN mRNA level were measured by real-time PCR. Transfection of ZEB1 siRNA, EZH2 siRNA and other plasmids were carried out by using Lipofectamine 2000. Chromatin Immunoprecipitation (ChIP) assay was performed using the ChIP assay system. Luciferase reporter gene assay was carried out using the Dual-Glo® Luciferase Assay

System following the manufacturer’s protocol. Results: Knockdown of EZH2 induced the formation of autophagesomes in colorectal cancer cell lines HCT116 and SW620, which was evident on electron microscopy. Furthermore, Western 上海皓元医药股份有限公司 Blot and real-time PCR data showed that ZEB1 and EZH2 may regulate the expression of PTEN, which plays a vital role in autophagy. Moreover, downregulation of ZEB1 significantly reduced the expression of EZH2. A highly inverse correlation between the expression of EZH2 and ZEB1 and that of PTEN was also revealed in CRC tissues compared with normal tissue in patients Conclusion: we firstly revealed the impact of EZH2 on autophagy during CRC carcinogenesis. At the same time, we firstly identified that EZH2 expression may be regulated by ZEB1 in colorectal cancer.