DRAM1 regulates the migration and invasion of hepatoblastoma cells via autophagy-EMT pathway.

DNA-damage regulated autophagy modulator 1 (DRAM1) is known as a target of TP53-mediated autophagy, and has been reported to promote the migration and invasion abilities of glioblastoma stem cells. However, the precise contribution of DRAM1 to cancer cell invasion and migration, and the underlying mechanisms remain unclear. In the present study, small interfering (si)RNA or short hairpin RNA mediated knockdown of DRAM1 was performed in hepatoblastoma cells and the migration and invasion abilities were detected in vitro and in vivo. To investigate the underlying mechanisms, western blotting and immunofluorescence were used to detect the expression of autophagy-associated proteins and epithelial-mesenchymal-transition (EMT)-associated markers. The results showed that DRAM1 knockdown by specific siRNA abrogated cell autophagy, as well as inhibited the migration and invasion of HepG2 cells in Transwell assays, which may be reversed by rapamycin treatment. In addition, DRAM1 knockdown increased the expression of E-Cadherin while decreased the expression of vimentin in HepG2 cells, which was also be reversed by rapamycin treatment. Taken together, these results suggest that DRAM1 is involved in the regulation of the migration and invasion of HepG2 cells via autophagy-EMT pathway.

MicroRNA gene polymorphisms and the risk of colorectal cancer.

The present study was carried out to demonstrate the epidemiological value of microRNA (miRNA) in colorectal cancer (CRC) by investigating the association between miRNA gene polymorphisms and the susceptibility to CRC. Multiple meta-analyses of reported data were conducted, and odds ratio values and 95% confidence intervals were used to assess these associations. Stata 11.0 software was used to analyze the data and the modified Jadad quality score was employed to evaluate the quality of the retrieved studies. We retrieved 38 studies on the association between miRNA polymorphisms and risk of CRC, however only 15 met the requirements of the inclusion criteria. In conclusion, we identified a variety of miRNAs (miRNA-let-7, miR-34b/c, miR-146a, miR-603 and miR-149) gene polymorphisms that are associated with susceptibility to CRC. However, some miRNAs (miR-192a, miR-608 and miR-27a) are associated with CRC, but not susceptibility to CRC. The results have limitations given the relatively low number of studies available. Therefore, it is necessary to collect data from large sample-size studies to further validate the results.

Hybrid Approaches for Complex Parastomal Hernia Repair.

Parastomal hernia is one of the major complications of colostomy with high occurrence. From October 2011 to November 2014, a retrospective study was conducted by analyzing and following up data of 16 patients suffering from parastomal hernia who underwent a hybrid technique repair. The safety and efficacy of the hybrid technique for parastomal hernia repair was investigated in terms of complications. All cases were operated successfully and had no major immediate postoperative complications other than mild abdominal pain in 5 cases. No long-term postoperative complications were reported in the follow-up. The authors found hybrid technique to be safe and effective for parastomal hernia repair with fewer complications.

TIGAR regulates DNA damage and repair through pentosephosphate pathway and Cdk5-ATM pathway.

Previous study revealed that the protective effect of TIGAR in cell survival is mediated through the increase in PPP (pentose phosphate pathway) flux. However, it remains unexplored if TIGAR plays an important role in DNA damage and repair. This study investigated the role of TIGAR in DNA damage response (DDR) induced by genotoxic drugs and hypoxia in tumor cells. Results showed that TIGAR was increased and relocated to the nucleus after epirubicin or hypoxia treatment in cancer cells. Knockdown of TIGAR exacerbated DNA damage and the effects were partly reversed by the supplementation of PPP products NADPH, ribose, or the ROS scavenger NAC. Further studies with pharmacological and genetic approaches revealed that TIGAR regulated the phosphorylation of ATM, a key protein in DDR, through Cdk5. The Cdk5-AMT signal pathway involved in regulation of DDR by TIGAR defines a new role of TIGAR in cancer cell survival and it suggests that TIGAR may be a therapeutic target for cancers.

Totally laparoscopic gallbladder-preserving surgery: A minimally invasive and favorable approach for cholelithiasis.

The aim of the present study was to investigate the effectiveness of laparoscopic gallbladder-preserving surgery (L-GPS) for cholelithiasis and the feasibility and value of totally laparoscopic GPS (TL-GPS). A total of 517 patients underwent L-GPS, including 365 cases of laparoscopy-assisted GPS (LA-GPS), 143 cases of TL-GPS (preservation rate, 98.3%) and nine conversions to laparoscopic cholecystectomy. The surgeries were all performed by one medical team and the mean operating time was 72 min. All macroscopic calculi were removed through endoscopy. The number of calculi observed in the patients was between one and several dozen; diameters ranged between 0.1 and 2.5 cm. Only three cases of incisional infection were noted in the LA-GPS group and long-term follow-up showed a low recurrence rate of 1.2%. L-GPS is, therefore, an excellent approach to cure cholelithiasis and TL-GPS is a feasible and effective option that could avoid incisional complications.

TIGAR has a dual role in cancer cell survival through regulating apoptosis and autophagy.

The p53-induced glycolysis and apoptosis regulator (TIGAR) inhibits glycolysis, resulting in higher intracellular NADPH, lower reactive oxygen species (ROS) and autophagy activity. In this study, we investigated whether TIGAR might exert dual impacts on cancer cell survival based on its ability to inhibit both apoptosis and autophagy. In liver or lung cancer cells treated with the anticancer drug epirubicin, TIGAR levels increased in a dose- and time-dependent manner. TIGAR silencing enhanced epirubicin-induced elevations in ROS levels and apoptosis rates, in a manner that was blocked by ectopic addition of NADPH or N-acetyl cysteine. These findings were correlated with reduced tumorigenicity and increased chemosensitivity in mouse xenograft tumor assays. In parallel, TIGAR silencing also enhanced the epirubicin-induced activation of autophagy, in a manner that was also blocked by ectopic addition of NADPH. Notably, TIGAR silencing also licensed epirubicin-mediated inactivation of the mTOR pathway, suggesting TIGAR also exerted a negative impact on autophagy. However, genetic or pharmacologic inhibition of autophagy increased epirubicin-induced apoptosis in TIGAR-silenced cells. Overall, our results revealed that TIGAR inhibits both apoptosis and autophagy, resulting in a dual impact on tumor cell survival in response to tumor chemotherapy. Cancer Res; 74(18); 5127-38. ©2014 AACR.

B­cell translocation 1 gene inhibits cellular metastasis­associated behavior in breast cancer.

B-cell translocation gene 1 (BTG1) is a member of the BTG/transducer of ERBB2 family, which regulates cell cycle progression in a variety of cell types and may have a role in inhibiting proliferation, promoting apoptosis and stimulating cellular differentiation in numerous cell types. However, the role of BTG1 in cancer metastasis is yet to be elucidated. In the present study, analysis of clinical specimens revealed that BTG1 mRNA levels were lower in lymph node metastases than those in benign breast tumors and normal human breast tissue. The effect of BTG1 on the metastatic behavior of breast cancer cells following stable transfection with a BTG1 expression vector was also investigated. The overexpression of BTG1 was observed to inhibit cell adhesion, migration and invasion. Furthermore, the overexpression of BTG1 was found to be involved in the inhibition of the metastasis-related proteins matrix metalloproteinase-2 and -9, as well as the promotion of the cell-cell adhesion-associated protein E-cadherin. In syngeneic nude mice breast tumor models, hepatic metastasis and angiogenesis were observed in the mice injected with the control cells, but not in those injected with pcDNA3-BTG1 cells. Immunohistochemistry revealed that overexpression of BTG1 decreased vascular endothelial growth factor expression in tumors. To the best of our knowledge, this is the first study to show that BTG1 overexpression decreases migration and invasion of breast cancer cells and thereby inhibits distant metastasis in mice breast tumor models.

Disturbance of autophagy-lysosome signaling molecule expression in human gastric adenocarcinoma.

Autophagy is classified as type II programmed cell death and may participate in tumorigenesis. However, changes in autophagy-lysosome signaling and the relationship between the apoptotic cascade and gastric cancer cells have not been fully elucidated. The present study investigated the induction of autophagy in poorly differentiated human gastric adenocarcinoma. Immunoblotting revealed markedly induced autophagy in low grade differentiated gastric adenocarcinoma, indicated by elevation of microtubule-associated protein 1 light chain 3-I/II conversion and Beclin 1 in human gastric carcinomas. In addition, the diffuse (poorly differentiated) subtype showed significantly elevated Lamp2 and cathepsin B protein levels. Concomitantly, significant induction of anti-apoptotic events were indicated by changes in B-cell lymphoma 2 (Bcl-2) and X-linked inhibitor of apoptosis protein levels. Notably, confocal laser microscope data indicated co-expression of Bcl-2 and Beclin 1 in poorly differentiated human gastric adenocarcinoma. Results of this study indicate that the autophagy-lysosome signaling participates in poorly differentiated human gastric adenocarcinoma and there are intracellular links between autophagic signaling and the apoptotic cascade.

Expression characteristics of CDC20 in gastric cancer and its correlation with poor prognosis.

The cell division cycle 20 homolog (CDC20) expression is increased in diverse human cancers and plays a vital role in tumorigenesis and progression. However, the clinical significance of CDC20 expression in gastric cancer (GC) remains largely unknown. The aim of this study was to investigate the clinicopathologic features and prognostic significance of CDC20 in GC. The CDC20 mRNA expression was measured by quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR). Immunohistochemistry (IHC) was used to detect the expression of CDC20 protein in 131 clinicopathologically characterized GC cases. The relationship between CDC20 expression and clinicopathological features was analyzed by appropriate statistics. Kaplan-Meier analysis and Cox proportional hazards regression models were used to investigate the correlation between CDC20 expression and prognosis of GC patients. The relative mRNA expression of CDC20 were significantly higher in GC tumor tissues than in the corresponding noncancerous tissues (P<0.001). Simultaneously, CDC20 protein expression was positively correlated with tumor size (P=0.02), histological grade (P=0.037), lymph node involvement (P=0.009), and TNM stage (P=0.015). Furthermore, Kaplan-Meier analysis indicated that patients with high CDC20 expression had poor overall survival (P<0.001). Multivariate analysis showed that high CDC20 expression was an independent predictor of overall survival. In conclusion, our data indicated that CDC20 upregulation was associated with aggressive progression and poor prognosis in GC. CDC20 was identified for the first time as an independent marker for predicting the clinical outcome of GC patients.

Blocking Bcl-2 leads to autophagy activation and cell death of the HEPG2 liver cancer cell line.

BACKGROUND: Apoptosis may be induced after Bcl-2 expression is inhibited in proliferative cancer cells. This study focused on the effect of autophagy activation by ABT737 on anti-tumor effects of epirubicin. METHODS: Cytotoxic effects of ABT737 on the HepG2 liver cancer cell line were assessed by MTT assay and cell apoptosis through flow cytometry. Mitochondrial membrane potential was measured by fluorescence microscopy. Monodansylcadaverin (MDC) staining was used to detect activation of autophagy. Expression of p53, p62, LC3, and Beclin1, apoptotic or autophagy related proteins, was detected by Western blotting. RESULTS: ABT737 and epirubicin induced growth inhibition in HepG2 cells in a dose- and time-dependent manner. Both ABT737 and epirubicin alone could induce cell apoptosis with a reduction in mitochondrial membrane potential as well as increased apoptotic protein expression. Further increase of apoptosis was detected when HepG2 cells were co- treated with ABT373 and epirubicin. Furthermore, our results demonstrated that ABT373 or epirubicin ccould activate cell autophagy with elevated autophagosome formation, increased expression of autophagy related proteins and LC3 fluorescent puncta. CONCLUSIONS: ABT737 influences cancer cells through both apoptotic and autophagic mechanisms, and ABT737 may enhance the effects of epirubicin on HepG2 cells by activating autophagy and inducing apoptosis.

Transcystic approach with micro-incision of the cystic duct and its confluence part in laparoscopic common bile duct exploration.

BACKGROUND: Laparoscopic transcystic common bile duct exploration has become a safe and ideal treatment of common bile duct stones. This study was designed to explore the clinical value of modified laparoscopic transcystic common bile duct exploration as a first line of treatment for patients with common bile duct stones. PATIENTS AND METHODS: A retrospective, case-control study of clinically comparable groups of patients who underwent the laparoscopic transcystic approach with micro-incision of the cystic duct and its confluence part in common bile duct exploration (LTM-CBD) (n=110) and laparoscopic common bile duct exploration (LCBD) (n=100) under the care of one surgeon was performed. All clinical data were analyzed retrospectively. RESULTS: There was no significant difference in terms of operation time between the two groups (P>.05). Postoperative hospital stay and abdominal drainage time were shorter in the LTM-CBD group than in the LCBD group (P<.05). Postoperative bile leakage was seen in 1 case (1 of 110) in the LTM-CBD group and 10 cases (10 of 100) in the LCBD group (P<.05). Twenty patients underwent T-tube drainage in the LCBD group, and primary closure was performed in the other patients; however, all cases in the LTM-CBD group underwent primary closure. The median follow-up was 12 months; 2 patients in the LCBD group who suffered from bile leakage presented with obstructive jaundice due to bile duct stenosis 6 months postoperatively. CONCLUSIONS: LTM-CBD, which can avoid postoperative T-tube drainage, decrease complications, shorten hospitalization time, and enhance the existing quality, is a minimally invasive, safe, and effective treatment.

Endoscopic subcutaneous mastectomy: A novel and effective treatment for gynecomastia.

The aim of this study was to evaluate the procedure for and efficacy of endoscopic subcutaneous mastectomy for gynecomastia. Endoscopic subcutaneous mastectomy was performed on 100 benign, palpable breast enlargements in 58 male patients who were followed-up for 15-63 months. The surgery was conducted with the insufflation of CO2 subdermally. No cases were converted to open surgery. The unilateral surgery time was 70-90 min. The mean volume of the resected tissue was 200 ml. All procedures were completed successfully, with satisfactory clinical effects and ideal esthetic results postoperatively. There were three cases (3%) of papillary epidermal partial necrosis; following removal of the dressing during the hospital stay, normal nipple sensation returned. Endoscopic subcutaneous mastectomy had good clinical effects and ideal cosmetic results and is an appropriate approach for gynecomastia.

[Values of magnetic resonance spectrum imaging in the diagnosis of hepatic fibrosis of rats].

OBJECTIVE: To explore the values of magnetic resonance spectrum (MRS) in early diagnosis, quantization analysis and staging of hepatic fibrosis. METHODS: A rat model of hepatic fibrosis was established by the method of carbon tetra carbon (CCl4). A total of 47 SD rats were divided into model (n = 40) and control (n = 7) groups. 1H-MRS was performed. The model rats of hepatic fibrosis were grouped according to their pathological stages. The ratio of peak height and peak area of metabolites and lipid (Cho/Lip, Glx/Lip, Lac/Lip and Cr/Lip) were calculated and compared respectively. RESULTS: The ratios of peak height of metabolites and lipid were as follows: ratio of Cho and Lip: significant differences existed between control and grades 3 and 4 model groups (P < 0.05); ratio of Glx and Lip: significant differences existed between control and grades 2, 3 and 4 model groups (P < 0.05); ratio of Cr and Lip: significant differences existed between control and grade 3 model groups (P < 0.05). The peak area ratio of main metabolites and lipid of liver were as follows: ratio of Cho and Lip: significant differences existed between control and grade 4 model groups (P < 0.05); ratio of Glx and Lip: significant differences existed between control and other groups (P < 0.05); ratio of Cr and Lip: significant differences existed between control and grade 4 model groups (P < 0.05); ratio of Lac and Lip: no significant differences existed between these groups (P > 0.05). CONCLUSION: The ratios of peak height and peak area of Cho/Lip, Glx/Lip and Cr/Lip are important for the staging of hepatic fibrosis.

Inhibition of proliferation of estrogen receptor­positive MCF­7 human breast cancer cells by tamoxifen through c­Jun transcription factors.

Activator of protein 1 (AP-1) is a heterodimeric transcription factor composed of various members of the Jun and Fos families and binds to DNA at specific AP-1 binding sites. AP-1 transcriptional activity is increased by phosphorylation at serine residues in the c­Jun component of AP-1. In the present study, the proliferation of MCF-7 breast cancer cells was found to be suppressed by tamoxifen (TAM)-activated c-Jun through the protein kinase C (PKC) pathway. The molecular mechanism by which c­Jun activation induces antiproliferative signals in estrogen receptor (ER)-positive MCF-7 human breast cancer cells remains unknown. TAM inhibited the proliferation of ER-positive MCF-7 human breast cancer cells and ER-negative MDA-MB-435 human breast cancer cells and 48 h incubation with 10 µM TAM led to inhibition of 80% of proliferation. In addition, no significant difference in c-Jun mRNA and protein levels was detected in MCF-7 and MDA-MB-435 cells stimulated by TAM for 48 h. TAM treatment of MCF-7 cells activated the transcriptional activity of AP-1, which responds specifically to phorbol ester. To determine the role of c-Jun in the antiproliferation of MCF-7 cells stimulated by TAM, the inhibition rates of MCF­7 cells were correlated with c­Jun expression and stimulation of TAM. Results showed that the inhibition rate of TAM-stimulated MCF-7 cells was positively regulated by overexpression of c-Jun and negatively regulated by underexpression of c-Jun. Overall, these results indicate that the TAM-stimulated antiproliferation of MCF-7 cells is positively regulated by c-Jun through activation of the PKC pathway.

[Injury repairing and magnetic resonance tracing of transplanted bone marrow stromal cells in rat liver with hepatic fibrosis].

OBJECTIVE: To explore the recurring patterns of migration and distribution of transplanted bone marrow stromal cells (BMSCs) in rat model with hepatic fibrosis and the feasibility of magnetic resonance (MR) tracing. METHODS: BMSCs labeled with 5-bromodeoxyuridine (Brdu) and super para-magnetic iron oxide (SPIO) were transplanted into rat model with hepatic fibrosis via portal vein. MR scan was performed at Hour 2, Day 3, Day 7 and Week 2 post-transplantation to analyze the hepatic features of MR signal intensity and pathohistology of BMSCs. RESULTS: Multiple hypo-intense lesions appeared in hepatic hilar region at Hour 2 and became smaller with the elapsing time. Hemosiderin and Brdu immunohistochemical stains showed that positive cells were found in portal vein of hepatic porta at Hour 2, small branches of portal vein, sinus hepaticus and around central veins of hepatic lobules at Day 3 and liver parenchyma (esp. in area of lesion) at Day 7 and Week 2. Some of transplanted BMSCs were tightly connected with liver cell to form liver cell cord. The signal intensity changes of MRI corresponded to histological findings at different timepoints. CONCLUSION: The transplanted BMSCs are gradually scattered in whole liver (esp. in lesion area) so that it may help to repair hepatic lesions. And the recurring patterns of MR signal intensity changes reflected the condition of distribution, immigration and differentiation of transplanted cells.

[Value of contrast-enhanced ultrasound imaging in monitoring malignant tumor during argon-helium cryosurgery].

OBJECTIVE: To assess the value of contrast-enhanced ultrasound imaging in monitoring the therapeutic effect of argon-helium cryosurgical treatment of malignant tumors. METHODS: Before and after argon-helium cryosurgical treatment, 42 patients underwent contrast-enhanced ultrasound imaging, conventional ultrasound imaging and enhanced CT or magnetic resonance imaging (MRI) for examining the number of tumor foci and the size of necrotic areas. RESULTS: A total of 80 tumor lesions were detected by contrast-enhanced ultrasound imaging. Compared with conventional ultrasound imaging, contrast-enhanced ultrasound imaging detected a significantly greater number of tumors and the intratumoral necrotic areas (96 vs 19) as well as a significantly increased mean size of necrotic areas (5.7∓3.6 cm vs 2.8∓1.7 cm), showing no significant differences from the results by enhanced CT and MRI (94 and 5.5∓3.3 cm, P=0.872 and 0.978, respectively). The short-term therapeutic effect of argon-helium cryosurgery evaluated by contrast-enhanced ultrasound imaging were also similar to that assessed by enhanced CT or MRI (P=0.906). CONCLUSION: Contrast-enhanced ultrasound imaging has important values in monitoring malignant tumors during argon-helium cryosurgical treatment and in evaluating the short-term therapeutic effect of the treatment.

Proteomic-based analysis for identification of potential serum biomarkers in gallbladder cancer.

Gallbladder cancer is the most common malignant tumor of the biliary tract. Early diagnosis of gallbladder cancer is difficult because of the latent onset and lack of good biomarkers. To identify new biomarkers that improve the early diagnosis and/or serve as possible therapeutic targets in gallbladder cancer is essential. In the present study, serum proteins were separated by two-dimensional gel electrophoresis (2-DE) in 3 patients with gallbladder cancer and 3 healthy volunteers. The differentially expressed spots were identified by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF-MS). Western blotting and immunohistochemistry were performed to verify the expression of certain candidate proteins. Protein expression and clinical correlation was evaluated. We found that 64 protein spots were significantly changed in gallbladder cancer. Twenty-four proteins including S100A10, haptoglobin, cystatin-B, profilin-1 and superoxide dismutase were successfully identified. Among these proteins, S100A10 and haptoglobin were validated using Western blotting. Immunohistochemically, the expression of S100A10 and haptoglobin proteins was found to be higher in gallbladder cancer tissues compared to that in gallbladder adenoma, liver cholangiocarcinoma and cholecystitis tissue. Patients with high expression of S100A10 and haptoglobin were linked to late stage disease and poor clinical prognosis. Our data suggest that combined comparative proteomic analysis by 2-DE and MALDI-TOF-MS is an effective method for identifying differentially expressed proteins in serum samples. These proteomic approaches could be used for identifying new serum biomarkers in gallbladder cancer. S100A10, haptoglobin and other identified proteins may be potential molecular targets for early gallbladder cancer diagnostics and therapeutic applications.

[Experimental study on the relationship between the ratio of length to width of slender narrow pedicle and random flap survival area in pig].

OBJECTIVE: To explore the relationship between the ratio of length to width of slender narrow pedicle and random flap survival area, and to provide a theoretical basis for the clinical application of slender narrow pedicle flaps. METHODS: 25 pigs were randomly divided into 5 groups, 5 pigs in each group. The ratio of length to width of slender narrow pedicle in 5 groups respectively was: 0:2, 1:2, 2:2, 3:2, 4:2. Every ratio' s slender narrow pedicle was carrying five different size of random flaps, which were 2 cm x 2 cm(A), 3 cm x 3 cm(B),4 cm x 4 cm(C), 5 cm x 5 cm(D), 6 cm x 6 cm(E), respectively. Flap A was control flap. In each group, flap A, B, C, D and E were created in each pigs' bilateral back. The order in both sides back is contrary. The flaps were evaluated with the general observation, fluorescence examination, blood flow ECT test, pathological expression and computerized analysis of survival area. RESULTS: (1) The living process and pathologic process of traditional flap and slender narrow pedicle flap were consistent. It could not postpone the flap living process when the flap pedicle became long and narrow. (2) When the ratio of the length to width of the slender narrow pedicle was constant, along with the flap area increased, the flap survival area also increased, but when the flap reached a certain area , the distal flap would necrosis,the flap survival area would not reduce. (3) When the flap size remained unchanged, along with the ratio of the length to width of the slender narrow pedicle increased, the flap survival area was not affected, but when the ratio of the length to width of the slender narrow pedicle increased to a certain limit, distal flap would necrosis, the flap survival area would reduce. CONCLUSIONS: (1) Pedicle width of random flap can be much smaller than flap width. The ratio of pedicle width to flap length is far less than traditional ratio. (2) The pedicle of random flap can be designed as slender shape, so that the whole flap looks like "pingpang bat", which makes the narrow pedicle flap rotate easily. (3) A certain ratio of the length to width of a slender narrow pedicle has a maximum flap survival area, and increasing the flap size or ratio of the length to width of a slender narrow pedicle in a certain extent will not lead to flap necrosis.

[Proteomic study of gallbladder cancer, with special reference on the expression and significance of annexin A3].

OBJECTIVE: To explore the potential molecular targets for diagnosis and treatment of gallbladder cancer by analyzing and comparing the proteomes expressed in human gallbladder cancer and benign gallbladder tissues. METHODS: The proteins expressed were analyzed using two-dimensional gel electrophoresis. The differentially expressed proteins in tumors were also analyzed by mass spectrometry (MS). AnnexinA3 expression was examined by streptavidin peroxidase immunohistochemical technique on paraffin-embedded tissue sections from 50 patients of gallbladder cancer and 38 cases of chronic eholecystitis. RESULTS: Protein extracts of individual sample in each type of tissues were separated on two-dimensional gels. There were forty six differentially expressed proteins in the tissue samples of gallbladder cancer. Seventeen proteins were successfully identified by MS, in which nine proteins were overexpressed in tumors and the other eight proteins were underexpressed. The positive expression rates of annexinA3 in gallbladder cancer was significantly higher than that in chronic cholecystitis, and the difference was statistically significant (74.0% vs 21.1%, P < 0.01). In the gallbladder cancer, no correlation was obtained between annexinA3 and age, gender or histologicl type (P > 0.05), but overexpression of annexinA3 correlated significantly with those cases with a lower histological grading (40.0% vs 82.5%, P < 0.05); lymph node or distant metastasis (40.9% vs 100%, P < 0.05); or a shorter survival time after operation (50.0% vs 93.8%, P < 0.05). CONCLUSIONS: Significant discrepancies in protein expression exist among gallbladder cancer and benign gallbladder tissues. AnnexinA3 plays an important role in the initiation and progression of human gallbladder cancer.

Anti-human CD133 monoclonal antibody that could inhibit the proliferation of colorectal cancer cells.

CD133, a five-transmembrane molecule, has been found on many types of cancers and determined to be a cancer stem cell biomarker. In this study a functional anti-human CD133 MAb 6B6 was obtained, and the specificity of this MAb was verified by flow cytometry. This MAb effectively recognized the CD133 molecule expressed on a series of malignant cell lines. Immunohistochemistry staining showed the CD133 was expressed on colorectal tumor tissue. Furthermore, we demonstrated that MAb 6B6 could inhibit the proliferation of Caco-2 cells that were derived from a human colorectal carcinoma. This functional anti-human CD133 MAb provides a valuable tool for further study of biological functions of cancer stem cell that expressed CD133.