16 In vitro, CD49fHCD41H MKPs stimulate the development of CD49fD HeP. Moreover, in transwell cultures, hepatospecific

genes are up-regulated in immature CD49fD HeP in response to direct cell contact and CD49fHCD41H cell-derived soluble factors, Dabrafenib in particular VEGF-A, which is produced most strongly by CD49fHCD41H cells. In fact, although VEGFR2/KDR is weakly expressed at E11.5 ex vivo by CD49fD HeP, its expression is up-regulated in vitro after the addition of VEGF-A. MKs produce VEGF,28 which participates in the endothelial organization of the vasculature, vasculogenesis, and blood island formation, and fulfils other nonvascular roles in the morphogenesis of adult organs and stem cell niches.16, 29-31 In addition to their role in hemostasis, platelets, the Kinase Inhibitor Library manufacturer end product of MK differentiation, are involved in liver regeneration and hepatocyte proliferation through direct contact as well as the release of HGF, insulin

growth factor, and VEGF.32, 33 Indeed, they are also involved in several other biological processes, including the spread of hematogenic tumor cells,34 vessel remodeling in the newborn,35 and the separation of blood and lymphatic circulation during development.36, 37 In conclusion, the data presented here describe the precise phenotypic identification of embryonic CD49fHCD41H MKPs. Our findings propose interesting new tools to study the role of MKs in tissue regeneration and strongly support a role new for CD49fHCD41H MKPs in the development MYO10 of the FL, involving the action both of cellular contacts and VEGF-A. The authors thank Beatriz Palacios, Fernando Martínez, and Carmen Prado for their technical assistance and help with the animal care and Mark Sefton for his editorial assistance. Additional Supporting Information may be found in the online version of this article. “
“Autophagy is a homeostatic mechanism that regulates protein

and organelle turnover and uses the amino acids from degraded proteins to produce adenosine 5′-triphosphate (ATP). We investigated the activity of autophagy-associated pathways in liver regeneration after partial hepatectomy (PHx) in liver-specific autophagy-related gene 5 (Atg5) knockout (KO) mice. Liver regeneration was severely impaired by 70% PHx, with a reduction in postoperative mitosis, but a compensating increase in hepatocyte size. PHx induced intracellular adenosine triphosphate and β-oxidation reduction as well as injured cellular mitochondria. Furthermore, PHx in Atg5 KO mice enhanced hepatic accumulation of p62 and ubiquitinated proteins. These results indicated that reorganization of intracellular proteins and organelles during autophagy was impaired in the regenerating liver of these mice.

16 In vitro, CD49fHCD41H MKPs stimulate the development of CD49fD HeP. Moreover, in transwell cultures, hepatospecific

genes are up-regulated in immature CD49fD HeP in response to direct cell contact and CD49fHCD41H cell-derived soluble factors, Poziotinib manufacturer in particular VEGF-A, which is produced most strongly by CD49fHCD41H cells. In fact, although VEGFR2/KDR is weakly expressed at E11.5 ex vivo by CD49fD HeP, its expression is up-regulated in vitro after the addition of VEGF-A. MKs produce VEGF,28 which participates in the endothelial organization of the vasculature, vasculogenesis, and blood island formation, and fulfils other nonvascular roles in the morphogenesis of adult organs and stem cell niches.16, 29-31 In addition to their role in hemostasis, platelets, the selleck inhibitor end product of MK differentiation, are involved in liver regeneration and hepatocyte proliferation through direct contact as well as the release of HGF, insulin

growth factor, and VEGF.32, 33 Indeed, they are also involved in several other biological processes, including the spread of hematogenic tumor cells,34 vessel remodeling in the newborn,35 and the separation of blood and lymphatic circulation during development.36, 37 In conclusion, the data presented here describe the precise phenotypic identification of embryonic CD49fHCD41H MKPs. Our findings propose interesting new tools to study the role of MKs in tissue regeneration and strongly support a role new for CD49fHCD41H MKPs in the development Montelukast Sodium of the FL, involving the action both of cellular contacts and VEGF-A. The authors thank Beatriz Palacios, Fernando Martínez, and Carmen Prado for their technical assistance and help with the animal care and Mark Sefton for his editorial assistance. Additional Supporting Information may be found in the online version of this article. “
“Autophagy is a homeostatic mechanism that regulates protein

and organelle turnover and uses the amino acids from degraded proteins to produce adenosine 5′-triphosphate (ATP). We investigated the activity of autophagy-associated pathways in liver regeneration after partial hepatectomy (PHx) in liver-specific autophagy-related gene 5 (Atg5) knockout (KO) mice. Liver regeneration was severely impaired by 70% PHx, with a reduction in postoperative mitosis, but a compensating increase in hepatocyte size. PHx induced intracellular adenosine triphosphate and β-oxidation reduction as well as injured cellular mitochondria. Furthermore, PHx in Atg5 KO mice enhanced hepatic accumulation of p62 and ubiquitinated proteins. These results indicated that reorganization of intracellular proteins and organelles during autophagy was impaired in the regenerating liver of these mice.

The pathogen is morphologically barely distinguishable from Phyllactinia moricola. However, it exhibits several new morphological characteristics which 2–3 conidia could be formed in short chains at the apex of the conidiophores and the conidia could produce two germ tubes in any position. Phylogenetic analyses of ITS sequences show that the pathogen has a close genetic relationship with P. moricola and Ph. broussonetiae-kaempferi, two GS-1101 molecular weight species on hosts belonging to family Moraceae. However, the ITS differences between Japanese sequences and

the Chinese sequence derived from mulberry are greater than expected for a single species and suggest a cryptic species in China, but the present data are not sufficient for a final conclusion. Therefore, the Morus powdery mildew in Yunnan can currently only be classified as Phyllactinia sp. Morphological features, including conidial germination pattern of this powdery mildew are described in detail, and the local climatic conditions of the disease are analysed,

which will provide the base for finding an effective method, including bio-control, to control the disease under local conditions. “
“A this website real-time quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) was employed to investigate the transcriptional levels of putative defence genes expressed during postharvest storage of Actinidia chinensis‘Hort16A’ kiwifruit. Significant decreases (80% reduction) in normalized gene expression over time relative to the basal levels of gene expression at harvest in control fruit were observed for thaumatin-like protein (TLP), class IV acidic

chitinase, chalcone-flavonone isomerase (CHI) and glucan Telomerase endo-1,3-beta-glucosidase (β-1,3-glucosidase). Reduction in transcript abundance for these genes paralleled the significant increase in postharvest ripe rot disease incidence over time (P = 0.0008). Gene expression levels were approximately the same in control vs. inoculated fruit for all the four genes described above, except for β-1,3-glucosidase where expression was significantly greater (P = 0.007) in inoculated than in control fruit. For one of the genes of interest that we had studied by qRT-PCR, TLP, a small amount of protein was purified and assayed in vitro for activity against Cryptosporiopsis actinidiae and Phomopsis spp., the causal agents of ripe rots of ‘Hort16A’ kiwifruit. TLP from kiwifruit did not appear to be directly toxic to either pathogen. TLP does not prevent ripe rots, but it may be useful as a marker of resistance given the temporal correlation between decreased TLP and increased ripe rots that was demonstrated by qRT-PCR. “
“A method for long-term storage of spores of Phakopsora pachyrhizi was optimized.

Example of selected papers INR: International Normalized Ratio, Pit: Platelets, GIB: Gastrointestinal Bleeding Disclosures: Saleh Alqahtani – Advisory Committees or Review Panels: Gilead Sciences, Jans-sen Therapeutics; Grant/Research Support: Merck & Co, Inc. The following people have nothing to disclose: Matthew J. McConnell, Ruben Hernaez, Sarah Sewaralthahab

Purpose: To evaluate the safety and clinical outcomes of MK0683 nmr BRTO and CARTO in the treatment of bleeding gastric varices and hepatic encephalopathy (HE). BRTO and CARTO have only recently gained acceptance in the U.S. They have been shown to be effective in controlling gastric variceal bleeding with low rebleed rates. In these techniques, sclerosant is infused into gastric varices after variceal outflow is obstructed with either a balloon (BRTO) or with coil embolization (CARTO). Methods: We describe six patients that underwent BRTO or CARTO from June 2013 to May 2014. Prior to procedure, patients had endoscopy which led to the diagnosis of gastric varices, and evaluated the presence of esophageal varices. Patients also underwent cross sectional abdominal imaging to evaluate vascular anatomy and the presence

of a portosystemic shunt. Procedures were performed using a foam mixture of air, 3% sodium tetradecyl sulfate, and ethiodized oil. Primary clinical endpoints included obliteration of varices, freedom from recurrent bleeding, survival and change in MELD score. Patients were monitored with endoscopy and cross sectional imaging. Results: We performed 7 sessions LDK378 chemical structure of BRTO or CARTO in 6 patients (mean age 59.5, 33% female, MELD scores range 9-23). 4 sessions of BRTO and 3 sessions of CARTO were performed. In 5 patients, the indication was bleeding gastric varices and in 1 patient, for refractory HE. In all patients, placement of TIPS

was either triclocarban unsuccessful or contraindicated (Table 1). Technical success was achieved in 6 of 6 patients (100%) and one patient required two sessions of BRTO. Average MELD score decreased from 14 to 7.5 at 3 months post procedure. All patients were without recurrent variceal bleeding. The patient who underwent BRTO for HE was without recurrent HE at 9 months follow-up. Conclusion: BRTO and CARTO were relatively safe and effective techniques to prevent recurrent gastric variceal bleeding and improve symptoms of HE. They are only beginning to gain popularity in the U.S. These procedures can be used in patients who have contraindications to TIPS and have the benefit of preserved liver function with a decrease in hepatic encephalopathy. Patient Characteristics and Results Disclosures: Dilip Moonka – Advisory Committees or Review Panels: Gilead; Grant/Research Support: Bristol-Myers Squibb, Genentech; Speaking and Teaching: Merck, Genentech, Gilead Syed-Mohammed R. Jafri – Advisory Committees or Review Panels: Gilead The following people have nothing to disclose: Lisa N.

32 Moreover, Pol and X have been shown to be able to counteract the pattern recognition receptor signaling in hepatocytes.8, 33, 34 Therefore, we speculated that nonparenchymal liver cells may contribute to intrahepatic ISG expression during HBV infection, selleck though the mechanisms involved are yet to be determined. In addition, although HBsAg did not influence IFN signaling in vitro, we cannot neglect the role of it and

hepatitis B e antigen in contributing to the IFN response defect in vivo, as they were reported to suppress Toll-like receptor–induced IFN-β and ISG induction in both the parenchymal and nonparenchymal liver cells.35 In addition, the data obtained from liver biopsies revealed that the nuclear translocation of STAT1/2 was impaired in HBV-positive cells, but was still intact in many neighboring cells without HBV infection. Therefore, comprehensive analysis of the interaction between HBV and the IFN system in both hepatocytes and nonparenchymal cells is necessary, PF-02341066 cell line and it will be interesting to compare the STAT activation pattern in different types of liver cells between the IFN responders and nonresponders to further explore factors affecting response to IFN-α therapy. Viruses have evolved various strategies to circumvent the IFN response, thus allowing them to escape the host defenses.36 HCV, for example, impairs type I

IFN response by blocking different levels of IFN-α signal pathway via its core, NS3 and NS5A Celastrol proteins. For HBV, we propose a two-part mechanism by which Pol inhibits the IFN-α–stimulated antiviral responses. These findings, together with our previous finding that Pol can inhibit the type I IFN induction,8 suggest that Pol is a multifunctional IFN antagonist. This knowledge not only helps us understand the mechanisms of resistance of HBV-infected patients to IFN treatment, it also clarifies the role of Pol in HBV persistence. Once viral replication reaches high levels, Pol may exert its anti-IFN activities to ensure the survival

of the virus. Notably, the sensitivity to IFN-α differs between HBV and HCV. It was reported that IFN treatment resulted in a rapid reduction in HCV but a moderate reduction in HBV.37 HBV seems to have a stronger ability to interfere with the IFN antiviral actions compared with HCV. However, the inhibitory effect of HBV on the IFN-α–mediated ISG induction was found to be modest.37 HBV, as a hepatotropic DNA virus, may have low sensitivity to IFN-induced ISGs and counteract the IFN actions at different levels, including the IFN signal transduction and antiviral functions of ISG products. Nevertheless, future studies are required to fully understand HBV resistance to IFN-α and precisely define the mechanisms by which IFN-α inhibits HBV replication.

In the cases of sepsis, it is possible that

the NSBB-induced reduction in cardiac output would have made these patients less able to cope with the further vasodilatation caused by sepsis,11 because reduction in cardiac output has been shown to be associated with increased incidence of potentially fatal renal failure in patients with spontaneous bacterial peritonitis (SBP).12 It is interesting that none of the patients died from cardiovascular or pulmonary dysfunction, which would be expected from NSBB use. Third, it is possible that the patients were not consecutively Sorafenib order enrolled, especially because approximately half of patients enrolled did not have varices despite belonging to Child-Pugh class C. The patients on NSBB appeared slightly sicker, with higher bilirubin, lower albumin, and lower serum sodium, and more patients had Child-Pugh class C cirrhosis. Although individually,

none of these parameters was significantly different from the non-NSBB group, it is difficult to assess whether the cumulative see more effects of all markers of hemodynamic abnormality and liver dysfunction would not have made the NSBB group more likely to succumb to their advanced cirrhosis. Although all these methodological issues could have affected the statistical estimations and the applicability of these results to daily medical practice, the authors have raised an important question concerning the safety of propranolol in patients with cirrhosis and refractory ascites. From a physiological standpoint, the pathogenesis of refractory ascites is related to an intense hemodynamic derangement involving Tau-protein kinase both the splanchnic and the systemic circulations. In the presence of high portal pressure, splanchnic vessels dilate and splanchnic pooling occurs, whereas the blood volume in the systemic circulation is relatively insufficient as a result of systemic arterial vasodilatation.13 Patients with

cirrhosis and refractory ascites are characterized by low systemic blood pressure and reduced renal perfusion with low glomerular filtration progressing to type 2 hepatorenal syndrome (HRS) (Fig. 1). Such patients are also susceptible to complications such as sepsis including SBP, hepatic encephalopathy, and type 1 HRS. Therefore, one may suggest that propranolol, which has a hypotensive effect, could be detrimental for patients with refractory ascites and hemodynamic instability. This is precisely why the authors suggested that the development of post-paracentesis circulatory dysfunction could have contributed to the increased mortality among the propranolol group, although they did not provide any evidence in the report. Finally, the potential negative effects of propranolol on “cirrhotic cardiomyopathy”, which is common in patients with advanced cirrhosis,14 could have also contributed to the increased mortality.

4A). It is yet to be determined whether the reduced inflammatory response in TLR4−/− mice was responsible for retardation of compensatory proliferation. Therefore, we generated TLR4-chimeric mice using irradiation and bone-marrow transplantation (BMT). Successful BMT in all mice was confirmed

selleck chemicals by assessing expression of TLR4 using genomic DNA from tail, blood, bone marrow (Fig. 4B). Expression of TLR4 on Kupffer cells (CD11b+) isolated from the chimeric mice was demonstrated by flow cytometry (Supporting Information Fig. 5). As expected, chimeric mice containing TLR4−/− bone marrow showed a significant reduction in TNFα and IL-6 production in the livers in response to DEN compared to mice transplanted with wt bone marrow (Fig. 4C), and the

levels of circulating TNFα and IL-6 were also lower in chimeric mice containing TLR4−/− bone marrow (Fig. 4D). In contrast, chimeric mice containing Carfilzomib purchase TLR4-wt bone marrow, but TLR4−/− resident liver cells (wt/TLR4−/−), had markedly elevated inflammatory responses relative to TLR4−/−/TLR4−/− mice. The restoration of inflammatory activation in TLR4−/− mice coincided with the presence of extended areas of epithelial proliferation, as visualized by immunohistochemical staining for Ki-67 (Fig. 4E). Kupffer cells are the main targets of LPS in the liver, and they have a pivotal role in the induction of TNFα and IL-6. As inactivation of Kupffer cells has been shown to Tolmetin cause a significant reduction in cytokine production and complementary proliferation in response to DEN,14 these data clearly indicate that TLR4 in Kupffer cells was generally required for inflammatory cytokine production and compensatory proliferation in

response to DEN exposure. NF-κB is involved in signal transduction of various extracellular stress stimuli including DEN treatment14 and regulates both proinflammatory and protective responses in the liver.19,20 We detected a marked decrease in nuclear staining of NF-κB, which is predominantly adjacent to the centrilobular area, in livers of DEN-treated-TLR4−/− mice compared to DEN-treated wt mice (Fig. 5A). ChIP assay revealed reduced binding of NF-κB to the promoter regions of its downstream genes including Bcl-xl, A20 and MnSOD(Supporting Information Fig. 6A) in TLR4−/− mice than wt mice. Consistently, quantitative PCR analysis revealed evidently decreased expression of A20 and Bcl-xl(Fig. 5B). Previous results suggest that ROS production contributes to DEN-induced cell apoptosis, whereas NF-κB inhibits oxidative stress through controlling expression of Mn-superoxide dismutase (MnSOD), a mitochondrial enzyme that detoxifies superoxide anions.21 Indeed, TLR4−/− mice exhibited decreased expression MnSOD but not CuZnSOD(Fig. 5C). The levels of reduced glutathione (GSH), a major cellular antioxidant, were much lower in the livers of DEN-treated TLR4−/− mice than in similarly treated wt mice (Fig. 5D).

7), and western blotting (Supporting Fig. 12) in 10 pairs of clinical HCC samples. Compared to paired normal tissues, repression of miR-7 expression was detected in 7 of 10 HCC cases. In accord with miR-7 repression (average, 0.44-fold; range, 0.13- to 0.73-fold), the expression of PIK3CD (average, 2.6-fold; range, 1.4- to 4.6-fold), Akt (average, 2.7-fold; range, 1.3- to 5.5-fold), and mTOR (average, 4.1-fold; range, 1.8- to 7.2-fold) was up-regulated in all 7 HCC cases (Fig. 7). Correlation analysis indicated that PIK3CD expression was reduced, along with miR-7 overexpression, in these 10 pairs of HCC specimens (r2 = 0.725, Pearson’s chi-square test; Supporting Fig. 13). HCC remains one of the top

three causes of cancer death in the Asia Pacific region and is also a severe disease worldwide.18 In addition Alpelisib to conventional therapeutic strategies having promise as potentially curative therapies for patients with

early HCC,2 targeted therapies are currently being developed to interfere with the transduction of key signaling pathways19 or to inhibit VX-770 in vivo the function of tumor-specific molecules, such as tyrosine kinases,20 in HCC. In the last decade, miRNA has emerged as a critical regulator of carcinogenesis and tumor progression.3, 21 Changes in miRNA profiling are associated with almost all aspects of cancer biology, including cell proliferation and metastasis.22 Studies have shed light on tumor-targeting therapies using miRNAs as a novel diagnostic and therapeutic tool.23 In this study, we focused on miR-7, which has been demonstrated to suppress tumor growth in brain cancers24 and metastasis in breast cancer.10 Chou et al. recently found that miR-7 was overexpressed in lung cancer and was targeted to Ets2 repressor

factor, a tumor suppressor, to enhance the oncogenic properties of lung cancer. These findings indicated that miR-7 might function as an oncogenic miRNA in lung cancer.25 Given this finding, we sought to determine whether miR-7 plays a role in HCC.26 In this 4��8C study, we demonstrated that miR-7 inhibits tumorigenesis and cancer metastasis in HCC both in vitro and in vivo by blocking a novel miR-7 target, PIK3CD. This molecule is a major component of the PI3K pathway, which functions downstream of EGFR, and transduces signals through the PI3K/Akt pathway.27 Our results indicate that the growth of HCC cells is repressed by cell-cycle arrest, but not by inducing apoptosis, when miR-7 is overexpressed. We also found that overexpression of miR-7 significantly repressed the migratory capability of HCC cells and inhibited invasiveness. In vivo, tumor volume decreased by approximately 3.5-fold when QGY-miR-7 subclone cells were injected into mice, compared to injection with control cells. Additionally, a significant inhibition of extrahepatic metastasis from the liver to the lungs15 was observed after overexpression of miR-7.

We have proposed that this mechanism plays a major role in inducing tolerance to antigens expressed intra-hepatically, and hence is likely involved in liver transplant

tolerance and in the generation of ineffectual immune responses associated with the persistence of hepatotropic infections. The mechanisms underlying suicidal emperipolesis remain unclear, however potential learn more mediators of this pathway of autoreactive T cell destruction include autophagy, which occurs when intracellular substrates are sequestered into double membrane vesicles and are subsequently targeted to lysosomes for degradation. The autophagy process is necessary for the degradation of bulk protein aggregates, and is induced under conditions of starvation and cellular remodeling. Autophagosome formation requires Atg72. Hypothesis: The vesicles containing internalised autoreactive T cell fuse with autophagosomes, leading to degradation of their contents using the same pathways as autophagy. Aim: To determine if interruption of the autophagic machinery in the liver rescues intra-hepatically activated autoreactive see more T cells from destruction by suicidal emperipolesis. Method: We used C57BL/6 mice in which

Atg7 deficiency was induced ubiquitously or in hepatocytes only. Consistent with published data, inhibition of autophagy led to hepatomegaly in both models2. Results: Adoptive transfer of transgenic CD8 T cells that expressed a T cell receptor specific for the C57BL/6-expressed MHC class I molecule H-2Kb Selleck Staurosporine into these mice led to the efficient clearance of CD8 T cells and protection from autoimmunity in both systems. Efficient degradation of transferred transgenic CD8 T cells was detected using both flow cytometry and confocal

microscopy, occurred rapidly within 12 hours of transfer, and did not differ from rates of deletion observed in control animals in which the autophagy machinery was intact. Conclusion: The autophagic machinery is not critical for the death of autoreactive CD8 T cells in the liver. Alternate pathways mediating this process are currently under investigation. 1. Benseler V, Warren A, Vo M, Holz LE, Tay SS, Le Couteur DG, Breen E, Allison AC, Van Rooijene N, McGuffog C, Schlitt HJ, Bowen DG, McCaughan GW, and Bertolino P. Hepatocyte entry leads to the degradation of autoreactive CD8 T cells. PNAS 2011; 108: 16735–16740. 2. Komatsu M, Waguri S, Ueno T, Iwata J, Murata S, Tanida I, Ezaki J, Mizushima N, Ohsumi Y, Uchiyama Y, Kominami E, Tanaka K, and Chiba T. Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice. JBC 2005; 169: 425–434.

HERMAN, MALCOLM

V. BROCK Corresponding Author: PO ZHAO, MINGZHOU GUO Affiliations: Chinese PLA General Hospital; Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute; Oncology Center, Johns Hopkins University GS-1101 clinical trial Objective: To explore the possibility of DNA damage repair genes methylation as prognostic and chemo-sensitive markers in human gastric cancer. Methods: DNA methylation status of five DNA damage repair genes (CHFR, FANCF, MGMT, MLH1 and RASSF1A) was detected by nested methylation specific PCR in 102 paraffin-embedded gastric cancer samples. Chi-square or Fischer’s exact tests were used for evaluating the relationship of methylation status and clinic-pathological characteristics. Kaplan–Meier method and Cox proportional hazards models were employed to analyze

the association of methylation status with overall survival and chemo-sensitivity. Results: Promoter region hypermethylation was detected in 34.3% (35/102), 21.6% Palbociclib in vitro (22/102), 12.7% (13/102), 9.8% (10/102) and 0% (0/102) for CHFR, MLH1, RASSF1A, MGMT, and FANCF genes respectively. No association was found between methylation of CHFR, MLH1, RASSF1A, MGMT or FANCF with gender, age, tumor size, tumor differentiation, lymph node metastasis and TNM stage. In docetaxel treated gastric cancer patients, unsensitive to docetaxel was found in CHFR unmethylated patients by Cox proportional hazards model (HR 0.243, 95%CI 0.069–0.859, p = 0.028), and the overall survival is longer in CHFR methylated group compared with CHFR unmethylated group (log rank p = 0.036). In oxaliplatin treated gastric cancer patients, unsensitive to oxaliplatin was found in MLH1 methylated patients (HR 2.988, 95%CI 1.064–8.394, p = 0.038), and the overall survival is longer in MLH1 unmethylated group compared with MLH1 methylated group (log rank p = 0.046). Conclusion: CHFR is frequently methylated in human gastric cancer and CHFR methylation may serve as docetaxel sensitive marker. MLH1 methylation Resveratrol was related to oxaliplatin unsensitive gastric cancer patients. Key Word(s): 1. CHFR; 2. MLH1; 3. Methylation; 4. Gastric Cancer; Presenting Author: MIN WANG Additional Authors:

SHUO CHEN, YING QING, MINYING LIN, ZHUANGJI LUO, DONG WU, QINGYAN LI, WEI HAN, JIAN CHEN Corresponding Author: MIN WANG Affiliations: Qilu hospital, Shandong university Objective: Sulforaphane (SFN), which is highly enriched in cruciferous vegetables, has been studied for its cancer chemopreventive properties and ability to induce autophagy. UDP-glucuronosyltransferase (UGT) 1A induction is one of the mechanisms responsible for the cancer chemopreventive activity of SFN. Methods: The Caco-2 cells were divided into six experimental groups: the control, SFN, 3-MA, rapamycin, SFN/3-MA and SFN/rapamycin. The viability change of cells were assessed. Western blot was employed to detect the expression of microtubule-associated protein 1 light chain 3 (LC3).