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1.
Chinese Journal of Organ Transplantation ; (12): 152-159, 2023.
Artigo em Chinês | WPRIM | ID: wpr-994645

RESUMO

Objective:To explore the current status of surgery for portal hypertension to grasp current status and future development of surgery in China.Methods:This study is jointly sponsored by China Hepatobiliary & Pancreatic Specialist Alliance & Portal Hypertension Alliance in China (CHESS).Comprehensive surveying is conducted for basic domestic situations of surgery for portal hypertension, including case load, surgical approaches, management of postoperative complications, primary effects, existing confusion and obstacles, liver transplantation(LT), laparoscopic procedures and transjugular intrahepatic portosystemic shunt(TIPS), etc.Results:A total of 8 512 cases of portal hypertension surgery are performed at 378 hospitals nationwide in 2021.Splenectomy plus devascularization predominated(53.0%)and laparoscopy accounted for 76.1%.Primary goal is preventing rebleeding(67.0%) and 72.8% of hospitals used preventive anticoagulants after conventional surgery.And 80.7% of teams believe that the formation of postoperative portal vein thrombosis is a surgical dilemma and 65.3% of hospitals practiced both laparoscopy and TIPS.The major reasons for patients with portal hypertension not receiving LT are due to a lack of qualifications for LT(69.3%)and economic factors(69.0%).Conclusions:Surgery is an integral part of management of portal hypertension in China.However, it is imperative to further standardize the grasp of surgical indications, the handling of surgical operation and the management of postoperative complications.Moreover, prospective, multi-center randomized controlled clinical studies should be performed.

2.
Chinese Journal of Digestive Surgery ; (12): 167-180, 2023.
Artigo em Chinês | WPRIM | ID: wpr-990624

RESUMO

Lenvatinib mesylate is an oral receptor tyrosine kinase inhibitor against targets of vascular endothelial growth factor receptors 1-3, fibroblast growth factor receptors 1-4, platelet-derived growth factor receptor α, stem cell growth factor receptor, and rearranged during transfection, et al. Lenvatinib has been approved by the National Medical Products Administration of China on September 4,2018, for the first-line treatment of patients with unresectable hepatocellular carcinoma who have not received systematic treatment before. Up to February 2023, Lenvatinib has been listed in China for more than 4 years, accumulating a series of post-marketing clinical research evidences. Based on the clinical practice before and after the launch of lenvatinib and referring to the clinical experience of other anti-angiogenesis inhibitors, domestic multidisciplinary experts and scholars adopt the Delphi method to formulate the Chinese Expert Guidance on Overall Application of Lenvatinib in Hepatocellular Carcinoma after repeated discussions and revisions, in order to provide reference for reasonable and effective clinical application of lenvatinib for clinicians.

3.
Cancer Research on Prevention and Treatment ; (12): 800-807, 2023.
Artigo em Chinês | WPRIM | ID: wpr-984574

RESUMO

Tumor extracellular matrix (ECM) is the center component of tumor microenvironment (TME), ECM diversity constitutes the inherent heterogeneity of TME that contributes to tumor growth, dormancy, drug resistance, and metastasis. Discoidin domain receptor 1 is one of the ECM receptors that interact with multiple ECM ligands. It also regulates the occurrence and development of tumors. Accordingly, DDR1 plays an increasingly important role in the prevention, diagnosis, and treatment of cancer. In this review, we primarily summarize the research of ECM and its receptors with components, regulation, cell receptors, and signaling pathways in tumor progression.

4.
Chinese Journal of Ultrasonography ; (12): 685-690, 2019.
Artigo em Chinês | WPRIM | ID: wpr-754859

RESUMO

To investigate the safety and feasibility of indocyanine green ( ICG ) fluorescence staining guided by laparoscopic ultrasound guiding portal branch puncture approach in anatomical segmentectomy of the liver . Methods The clinical data of 22 patients with malignant liver diseases underwent anatomical segmentectomy between February 2018 and M ay 2018 were retrospectively analyzed . ICG 0 .125~0 .250 mg was directly injected into the portal branches supplying blood flow to the tumor‐bearing hepatic segment , after puncturing of the target portal branch under intraoperative laparoscopic ultrasound guidance in all patients . T he fluorescence imaging system ( Pinpoint) was used for the resection procedure . Observation indicators :intraoperative conditions ( tumor diameter ,success rate of portal branches puncture ,success rate of staining the target hepatic segment ,intraoperative complications , time of operation ,volume of intraoperative blood loss , blood transfusion , and transit of laparotomy ) . Postoperative conditions :postoperative complications ,and length of hospital stay . Results Twenty‐two patients with liver tumors were all performed anatomical hepatectomy assisted by laparoscopic ultrasound guiding ICG injection for liver segment staining . All the liver tumors were hepatocellular carcinoma . ①Intraoperative conditions : T he portal branches puncture successful rate was 100% ( 22/22 ) . Eighteen patients achieved expected effect of ICG fluorescence staining ,with a satisfaction rate of 81 .8% (18/22) and 4 failed to get expected effect ,including 2 with uneven dying ,and 2 with adjacent hepatic segmental staining induced to unclear boundary . No complication such as allergy occurred in all patients after ICG injection . T he mean operation time was ( 209 ± 89 ) min ( range :97 ~ 325 min) and the target portal branches ICG puncture injection time under intraoperative laparoscopic ultrasound guidance was ( 11 ± 5) min ( range 3-25 min) . T here was no intraoperative blood transfusion or transit of laparotomy .Average tumor diameter was ( 3 .9 ± 1 .3) cm( range :2 .2-7 .0 cm ) . ②Postoperative conditions of 22 patients ,4 with grade Ⅰ - Ⅱ of Clavien‐Dindo classification were improved by drug treatments ( 1 with deep venous thrombosis of the lower extremities and 3 with pleural effusion ) , no patient had grade Ⅲ and above complications , and no perioperative death occurred . Average duration of hospital stay was ( 7 ± 2 ) days in 22 patients ( range :5 .0-14 .0 days) . Conclusions ICG fluorescence staining guided by laparoscopic ultrasound guiding portal branch puncture ,obtains accurate and lasting fluorescence markers on the liver surface and inside the parenchyma . ICG staining guides the selection of liver section in the operation of liver in real time ,and helps surgeons to perform laparoscopic anatomical segmentectomy of the liver .

5.
Chinese Journal of General Surgery ; (12): 193-195, 2009.
Artigo em Chinês | WPRIM | ID: wpr-395842

RESUMO

Objective To evaluate the usefulness of the "inserting" bilio-jejunostomy for iatrogenic bile duct injury. Methods A retrospective analysis was performed on 27 cases with iatrogenic bile duct injury treated by the "inserting" bilio-jejunostomy in the past 11 years. Results Among the 27 patients, bile duct injury was caused by open cholecystectomy in 21 and by laparoscopic cholecystectomy in 6. The diameter of injuried bile ducts in all patients was less than 1 centimeter (0.3~0.8 cm ). The end of remnant bile duct 2~3 cm in length was completely inserted into the jejunum loop in 10 cases, while the anterior wall of the remnant bile duct inserted into jejunum loop with the posterior wall anastomosed with the jejumum conventionally in 17 cases. There was no biliary fistula nor stenosis occurred after the operation. Conclusions The "inserting" bilio-jejunostomy is a simple,safe and useful method, and this new surgical technique should be applied to patients with iatrogenic bile duct injury when bilio-enteric reconstruction was needed.

6.
Chinese Journal of Digestive Surgery ; (12): 204-208, 2009.
Artigo em Chinês | WPRIM | ID: wpr-394739

RESUMO

Objcctive To detect the telomerase activity in rat hepatic oval cells, and to explore the relationship between telomerase expression and the proliferation and differentiation of oval cells. Methods The 2-acetamidofluorene/partial bepatectomy (2-AAF/PH) rat model was used to induce the proliferation of oval cells. Oval cells were isolated by modified collagenase perfusion and gradient centrifugation. Electron microscope exami-nation and immunofluorescence were adopted to identify oval cells. Immunohistochemistry, RT-PCR and fluores-cence quantitative PCR were used to detect the expression of telomerase in oval cells. All the data collected were analyzed by t test. Results The proliferatiun of oval cells was successfully induced by 2-AAF/PH rat model. Freshly isolated oval cells showed a large and ovoid nuclei, a small proportion of cytomplasm and a cobblestone appearance. When viewed by electron microscopy, there were few and immature organelles, and the nucleus/ cytoplasm ratio was high. Immunofluorescence staining showed that oval cells expressed OV-6, alpha-fetoprotein, cytokeratin-19, albumin and c-kit. Telomerase reverse transcriptase (TERT) was located in the nuclei of oval cells which were around the portal areas. As oval cells differentiated into small hepatocytes, the number of TERT-positive cells decreased significantly. The expression level of TERT mRNA in normal rat liver tissue was 2.27 times higher than that in LE-6 oval cells; the expression level of TERT mRNA in the isolated oval cells was 1.26 times higher than that in LE-6 oval cells. The telomerase activity decreased gradually (from △A=1.05, 1.15 to △A=0.25, 0.45) as the increase of oval cells passage (from passage 24 to passage 40) (t=17.74, 12.38, P<0.05). Conclusions Oval cells have telomerase activity. Telomerase may be indispensable for maintaining the proliferative and multi-directional differentiation abilities of oval cells.

7.
Chinese Journal of General Surgery ; (12): 788-790, 2008.
Artigo em Chinês | WPRIM | ID: wpr-398269

RESUMO

Objective To study the effects of HIF-1α expression on the growth of subcutaneously implanted human hepatocellular carcinoma (HCC) cell lines in nude mice. Methods A nude mouse model of subcutaneously implanted HCC cell line HepG2Tet-on-HIF-1α was established. This cell lines characterizes the inducible expression of HIF-1α by doxycycline (Dos). The impact of HIF-1α expression induced by Dox on the growth of subcutaneously implanted HCC cell lines in the nude mouse model was observed. Results The mRNA and protein expression of HIF-1α were significantly up-regulated in the nude mouse model by oral administration of Dox. Compared with that model in which Dox was not administrated ie Dos( - ) group, the tumor volume(513.545 ± 276. 229) mm3 vs. ( 166. 506 ± 110. 142) mm3 ( P < 0. 05 ), tumor weight ( 1.251 ± 0. 438 ) g vs. (0. 640 ± 0. 296) g ( P < 0. 05 ), and tumor growth velocity were significantly enhanced in Dox ( + ) group, while tumor necrosis was inhibited ( 31. 360% ±2. 728% vs. 36. 640% ± 3. 804% ) (P<0. 05). The weight loss of nude mice was larger in Dox( + )group( P < 0. 01 ). There was no liver or lung metastasis in either group. Conclusion The expression of HIF-1αin subcutaneously implanted HCC in a nude mouse model is up-regulated by oral Dox. High grade expression of HIF-1α promotes the growth of implanted HCC.

8.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 173-5, 2007.
Artigo em Inglês | WPRIM | ID: wpr-634550

RESUMO

The roles of multi-drug resistance protein 1 (MDR1), multi-drug resistance related protein 1 (MRP1), lung resistance protein (LRP) and breast cancer resistance protein (BCRP) in the multi-drug resistance (MDR) of hepatocellular carcinoma (HCC) were studied. By exposing HepG2 cell line to progressively increased concentrations of adriamycin (ADM), HepG2 multi-drug resistant subline (HepG2/ADM) was induced. The MDR index of HepG2/ADM was detected by using MTT. The expressions of the four MDR proteins in the three cell lines (L02, HepG2, HepG2/ADM) were investigated at mRNA and protein levels by real-time RT-PCR and Western blot respectively. Our results showed that when the ADM concentration was under 100 microg/L, HepG2 could easily be induced to be drug-resistant. The IC(50) of the HepG2/ADM to ADM was 282 times that of HepG2. The expression of MDR1 and BCRP mRNA in HepG2/ADM cells were 400 and 9 times that of HepG2 cells respectively while there was no difference in the mRNA expressions of MRP1 and LRP. There was no difference between HepG2 and L02 cells in the mRNA expressions of the four genes. At the protein level, the expressions of MDR1, BCRP and LRP but MRP1 in HepG2/ADM were significantly higher than those of HepG2 and L02. Between HepG2 and L02, there was no difference in the expressions of four genes at the protein level. HepG2/ADM is a good model for the study of MDR. The four genes are probably the normally expressed gene in liver. The expressions of MDR1 and BCRP could be up-regulated by anti-cancer agents in vitro. The MDR of HCC was mainly due to the up-regulation of MDR1 and BCRP but MRP1 and LRP. These findings suggest they may serve as targets for the reversal of MDR of HCC.

9.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 173-175, 2007.
Artigo em Chinês | WPRIM | ID: wpr-317456

RESUMO

The roles of multi-drug resistance protein 1 (MDR1), multi-drug resistance related protein 1 (MRP1), lung resistance protein (LRP) and breast cancer resistance protein (BCRP) in the multi-drug resistance (MDR) of hepatocellular carcinoma (HCC) were studied. By exposing HepG2 cell line to progressively increased concentrations of adriamycin (ADM), HepG2 multi-drug resistant subline (HepG2/ADM) was induced. The MDR index of HepG2/ADM was detected by using MTT.The expressions of the four MDR proteins in the three cell lines (L02, HepG2, HepG2/ADM) were investigated at mRNA and protein levels by real-time RT-PCR and Western blot respectively. Our results showed that when the ADM concentration was under 100 μg/L, HepG2 could easily be induced to be drug-resistant. The IC50 of the HepG2/ADM to ADM was 282 times that of HepG2. The expression of MDR1 and BCRP mRNA in HepG2/ADM cells were 400 and 9 times that of HepG2 cells respectively while there was no difference in the mRNA expressions of MRP1 and LRP. There was no difference between HepG2 and L02 cells in the mRNA expressions of the four genes. At the protein level, the expressions of MDR1, BCRP and LRP but MRP1 in HepG2/ADM were significantly higher than those of HepG2 and L02. Between HepG2 and L02,there was no difference in the expressions of four genes at the protein level. HepG2/ADM is a good model for the study of MDR. The four genes are probably the normally expressed gene in liven The expressions of MDR1 and BCRP could be up-regulated by anti-cancer agents in vitro. The MDR of HCC was mainly due to the up-regulation of MDR1 and BCRP but MRP1 and LRP. These findings suggest they may serve as targets for the reversal of MDR of HCC.

10.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 448-50, 2006.
Artigo em Inglês | WPRIM | ID: wpr-634945

RESUMO

To study the role and mechanisms of hypoxia-inducible factor-1alpha (HIF-1alpha) on the growth and tumorigenicity of lung cancer cells A549, the antisense oligonucleotide of HIF-1alpha was transfected to A549 cells. The effect of the antisense oligonucleotide on tumor growth in vitro and in vivo was evaluated by the growth rate suppression of A549 cells and subcutaneous implanted tumor in nude mice, and the effect on tumorigenicity was evaluated by the expression inhibition of angiogenic factors, the microvessel density (MVD) and vascular endothelial growth factor (VEGF) protein expression which were detected by immohistochemistry and western blot respectively. This study revealed that in vitro the growth rate of antisense oligonucleotide group was significantly decreased as compared with that of control group, sense oligonucleotide group and false-sense oligonucleotide group; in vivo the weight of implanted tumors in nude mice of antisense oligonucleotide group was 1.51 +/- 0.40 g, which was significantly lower than that of control group (2.79 +/- 0.33 g), sense oligonucleotide group (2.81 +/- 0.45 g) and false-sense oligonucleotide group (2.89 +/- 0.39 g) and the inhibitory rate was 47%. Both MVD and VEGF protein expression were significantly inhibited in antisense oligonucleotide group compared with those in other groups. These results indicated that antisense oligonucleotide of HIF-1alpha could inhibit lung cancer cells A549 growth in vitro and in vivo, and the mechanism may be due to the inhibition of vascular growth and VEGF protein expression.

11.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 520-3, 2006.
Artigo em Inglês | WPRIM | ID: wpr-634406

RESUMO

In order to construct plasmid of hypoxia-inducible factor-1alpha (HIF-1alpha), and transfect into human lung cancer cells A549, the change in sensitivity of lung cancer cells A549 to chemotherapy was observed. HIF-1alpha mRNA structure region was amplified by RT-PCR and inserted into plasmid pcDNA3. The expression plasmid pcDNA3/HIF-1alpha was transfected into A549 with Lipofec-tAMINE2000. The expression of HIF-1alpha protein was detected by Western blot. After A549 cells were transfected with HIF-1alpha prior to addition of 5-Fu, the growth activity was measured by growth curve, apoptosis was detected by flow cytometry at 48 h, and the levels of caspase3 and MDR-1 were determined by Western blot. The results showed that the constructed expression plasmid was analyzed with restriction enzymes and gel electrophoresis. Two DNA lanes at 2.55 kb and 5.4 kb respectively were found, which were consistent with that expected. The growth rate in 5-Fu group was significantly inhibited, and the apoptosis index and caspase3 activity were increased significantly as compared with control group. After HIF-1alpha being transfected into A549, the activity of MDR-1 was increased and the effect of 5-Fu was weakened. In conclusion, HIF-1alpha can promote chemoresistance by increasing the activation of MDRI and suppressing apoptosis during lung cancer cells A549 induced with 5-Fu.

12.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 448-450, 2006.
Artigo em Chinês | WPRIM | ID: wpr-313437

RESUMO

To study the role and mechanisms of hypoxia-inducible factor-1alpha (HIF-1α) on the growth and tumorigenicity of lung cancer cells A549, the antisense oligonucleotide of HIF-1α was transfected to A549 cells. The effect of the antisense oligonucleotide on tumor growth in vitro and in vivo was evaluated by the growth rate suppression of A549 cells and subcutaneous implanted tumor in nude mice, and the effect on tumorigenicity was evaluated by the expression inhibition of angiogenic factors, the microvessel density (MVD)and vascular endothelial growth factor (VEGF) protein expression which were detected by immohistochemistry and western blot respectively. This study revealed that in vitro the growth rate of antisense oligonucleotide group was significantly decreased as compared with that of control group, sense oligonucleotide group and false-sense oligonucleotide group; in vivo the weight of implanted tumors in nude mice of antisense oligonucleotide group was 1.51±0.40 g, which was significantly lower than that of control group (2.79±0.33 g), sense oligonucleotide group (2.81±0.45g) and false-sense oligonucleotide group (2.89±0.39 g) and the inhibitory rate was 47 %. Both MVD and VEGF protein expression were significantly inhibited in antisense oligonucleotide group compared with those in other groups. These results indicated that antisense oligonucleotide of HIF-1α could inhibit lung cancer cells A549 growth in vitro and in vivo, and the mechanism may be due to the inhibition of vascular growth and VEGF protein expression.

13.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 520-523, 2006.
Artigo em Chinês | WPRIM | ID: wpr-313417

RESUMO

In order to construct plasmid of hypoxia-inducible factor-lalpha (HIF-1α), and transfect into human lung cancer cells A549, the change in sensitivity of lung cancer cells A549 to chemotherapy was observed. HIF-1α mRNA structure region was amplified by RT-PCR and inserted into plasmid pcDNA3. The expression plasmid pcDNA3/HIF-1α was transfected into A549 with LipofectAMINETM2000. The expression of HIF-1α protein was detected by Western blot. After A549 cells were transfected with HIF-1α prior to addition of 5-Fu, the growth activity was measured by growth curve, apoptosis was detected by flow cytometry at 48 h, and the levels of caspase3 and MDR-1 were determined by Western blot. The results showed that the constructed expression plasmid was analyzed with restriction enzymes and gel electrophoresis. Two DNA lanes at 2.55 kb and 5.4 kb respectively were found, which were consistent with that expected. The growth rate in 5-Fu group was significantly inhibited, and the apoptosis index and caspase3 activity were increased significantly as compared with control group. After HIF-1 α being transfected into A549, the activity of MDR-1 was increased and the effect of 5-Fu was weakened. In conclusion, HIF-1α can promote chemoresistance by increasing the activation of MDR1 and suppressing apoptosis during lung cancer cells A549 induced with 5-Fu.

14.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 75-78, 2006.
Artigo em Chinês | WPRIM | ID: wpr-266429

RESUMO

In order to investigate the inhibitory effects on the vascular endothelial growth factor (VEGF) expression and cell growth in hapatocellular carcinoma (HCC) by blocking HIF-1α and Smad3 binding site in the VEGF promoter, antisense oligodeoxynucleotides (ASODN) were designed to block HIF-1α and Smad3 binding site in the VEGF promoter. Different concentrations of ASODN and ODN were transfected into HCC cells respectively. The expression of VEGF mRNA and protein was detected by SABC, Western blot and RT-PCR techniques and the inhibitory effects on the expression of VEGF and cell growth of the HCC cells stimulated by the supernatants were determined by using MTT method. Immunohistochestry revealed that after co-inoculation of hepatocellular carcinoma cells with different concentrations of ODN and ASODN for 48 h, there was no significant difference in the expression of VEGF protein between ODN group and control group (P>0.05), but there was significant difference between ASODN group and control group (P<0.05). At a concentration of 10 μmol/L ASODN, the difference was very significant (P<0.01).Western blot and RT-PCR revealed that, after treatment for 48 h at a concentration of 10 μmol/L,the integral gray levels and RNA odds were 59743.2±10412.5 and 0. 783±0. 032 in ODN group,and 38694.5±10925. 1 and 0. 468±0. 015 in ASODN group, respectively, with the difference being very significant (P<0.01). Antisense ODN could inhibit the growth of HCC cells in a concentration-dependent manner. It was concluded that anti-gene technique of aiming at HIF-1α action site in the VEGF promoter could suppress the VEGF expression and inhibit HCC cell growth, and it is promising that anti-gene technique works as a new gene therapeutic tool for anti-angiogenesis of HCC.

15.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 36-39, 2006.
Artigo em Chinês | WPRIM | ID: wpr-234512

RESUMO

The effect and mechanism of the ciglitazone on lung cancer cells A549 growth in vitro and in vivo were studied. Various concentrations of ciglitazone were added to the cultured A549 line, and the proliferation and differentiation of A549 cells were examined by MTT and cytometry analysis. A549 cells (1 × 106/mouse) were inoculated subcutaneously into 20 nude mice, which were randomly divided into two groups: the control group, the ciglitazone treated group. The weights of subcutaneous tumors were measured. The expression of cyclin D1 and P21 in the lung was detected by immohistochemistry and Western blot respectively. The results showed that the proliferation of A549 was inhibited significantly by ciglitazone in a dose- and time-dependent manner. There were more cells arrested in G1/G0 phase and the expression of PPARγ was markedly upregulated in ciglitazone-treated group. Direct injection of ciglitazone into A549-induced tumors could suppress tumor growth in nude mice and the growth inhibitory rate was 36 %. The expression of cyclin D1 was decreased and P21 increased significantly in ciglitazone-treated group as compared with control group. It was concluded that ciglitazone could inhibit A549 proliferation dose-dependently and time-dependently and induce differentiation, which might be related to the modulation of cell cycle interfered by PPARγ.

16.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 51-54, 2005.
Artigo em Chinês | WPRIM | ID: wpr-336936

RESUMO

The therapeutic potential of soluble TRAIL (sTRAIL) in hepatocellular carcinoma(HCC) was studied. The expression of TRAIL receptors was detected in 60 HCC tissues, 20 normal liver samples and 2 HCC cell lines (HepG2 and SMMC-7721) by in situ hybridization. Before and after HepG2 and SMMC-7721 were treated with sTRAIL protein with various concentrations,the apoptosis rate was observed by using flow cytometry and in situ terminal deoxynucleotidyl tranferase (TdT) labeling. The results showed death receptor 4 (DR4) and DR5 were expressed in 60 HCC tissues and 20 normal liver samples, while the expression intensity of DR in HCC tissues was stronger than in normal liver samples. DcR1and DcR2 were not detectable in 54 (90 %) and 25 (41.7 %)HCC tissues, while in 20 normalliver samples, DcR was detectable. The high expressionof DR and low expression of DcR in HCC tissues were significantly differed from the low expression and high expression in normal liver samples. The expression of DR5, DR4 and DcR2 in both HCC cell lines was detectable, but the expression of DcR1 was not detectable. The expression of DR in HCC tissues was related to the differentiation and grades of HCC. In the poor differentiated HCC, the expression of DR was decreased (P<0.01). The expression of DR in Ⅲ/Ⅳ grades was significantly lower than that in Ⅰ / Ⅱ grades (P<0.05). The expression of DR was not related to gender, age, HBsAg, AFP, tumor sizeand metastasis. The expression of DR in the HCC drugresistant lines was decreased. After treatment with TRAIL (100 ng/ml) for 24 h, the apoptosis rate of HCC cells, Jurkat cells and human cholangiocarcinoma cell line QBC939 was 10 %, 70 %,50 % respectively. It was suggested that the TRAILR expression is prevalent in HCC with different expression patterns of different receptor types. HCC is resistant to TRAIL-mediated apoptosis.The treatment of TRAIL alone has a limited effect on inducing apoptosis of HepG2 and SMMC-7721.

17.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 585-587, 2004.
Artigo em Inglês | WPRIM | ID: wpr-336971

RESUMO

To investigate the expression of KLF6mRNA in primary hepatocellular carcinoma (HCC), nomal liver tissues and the tissues adjacent to the cancers, reverse-transcription polymerase chain reaction (RT-PCR) was employed to investigate the expression of the KLF6 gene in HCC, the corresponding adjacent non-cancerous tissues and normal liver tissue. Our results showed that an amplified fragment of 427 bp DNA was detected in 18 of 19 (94.7%) adjacent non-cancerous tissues and normal liver tissue, and in 12 (85.7%) of 14 HCC. There were no significant differences in the levels of KLF6 mRNA between normal liver and liver tumors (P>0.05). It is concluded that KLF6 mRNA is generally expressed in HCC.


Assuntos
Humanos , Carcinoma Hepatocelular , Metabolismo , Fator 6 Semelhante a Kruppel , Fatores de Transcrição Kruppel-Like , Genética , Fígado , Metabolismo , Neoplasias Hepáticas , Metabolismo , Proteínas Proto-Oncogênicas , Genética , RNA Mensageiro , Genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa
18.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 585-7, 2004.
Artigo em Inglês | WPRIM | ID: wpr-634192

RESUMO

To investigate the expression of KLF6mRNA in primary hepatocellular carcinoma (HCC), nomal liver tissues and the tissues adjacent to the cancers, reverse-transcription polymerase chain reaction (RT-PCR) was employed to investigate the expression of the KLF6 gene in HCC, the corresponding adjacent non-cancerous tissues and normal liver tissue. Our results showed that an amplified fragment of 427 bp DNA was detected in 18 of 19 (94.7%) adjacent non-cancerous tissues and normal liver tissue, and in 12 (85.7%) of 14 HCC. There were no significant differences in the levels of KLF6 mRNA between normal liver and liver tumors (P>0.05). It is concluded that KLF6 mRNA is generally expressed in HCC.


Assuntos
Carcinoma Hepatocelular/metabolismo , Fatores de Transcrição Kruppel-Like/biossíntese , Fatores de Transcrição Kruppel-Like/genética , Fígado/metabolismo , Neoplasias Hepáticas/metabolismo , Proteínas Proto-Oncogênicas/biossíntese , Proteínas Proto-Oncogênicas/genética , RNA Mensageiro/biossíntese , RNA Mensageiro/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa
19.
Chinese Journal of Bases and Clinics in General Surgery ; (12)2004.
Artigo em Chinês | WPRIM | ID: wpr-544505

RESUMO

Objective To investigate the expressions of platelet derived growth factor (PDGF) and survivin in hepatocellular carcinoma (HCC) with portal vein tumor thrombosis (PVTT) and to evaluate the relationships among the expressions of PDGF, survivin and the proliferation of cancer cells. Methods The expression of PDGF mRNA in 16 cases in HCC with PVTT group was observed by in situ hybridization and the results were compared with that in HCC tissue group. The expressions of PDGF and survivin protein in 36 cases in HCC with PVTT group were detected with immunohistochemistry and it was found that there was a correlation between them. Flow cytometry (FCM) was used to measure the proliferation of cancer cells and it was also used to analyze the relations among PDGF, survivin and the proliferation of cancer cells. Results The expression level of PDGF mRNA in HCC with PVTT group was significantly higher than that in HCC tissue group (P

20.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 383-386, 2003.
Artigo em Inglês | WPRIM | ID: wpr-330899

RESUMO

To investigate the effect of HBx on expression of survivin in hepatoma cells and mechanisms of inhibition of apoptosis on hepatoma cells induced by HBx, the expression plasmid pHA-HBx encoding full length of HBx was transfected into HepG2 cells and the transformed cells were identified by RT-PCR. The expression of survivin both in HepG2 cells and HBx-transfected cells was examined with RT-PCR. The nude mice model of hepatoma was established by injecting HepG2 cells and HBx-transfected cells into the flank of nude mice subcutaneously. The expression level of survivin both in HepG2 formed tumors and HBx-transfected cell-formed tumors in nude mice was examined with Western-blot. The TUNEL assay was used to detect the apoptotic cells of tumor tissues in nude mice after intraabdominal chemotherapy with adriamycin. The results indicated that the amplification of survivin in HBx-transfected HepG2 cells was up-regulated when compared with that in non-transfected cells. Western-blot showed that the tumor cells expressing HBx in nude mice had a positive band of survivin expression and the tumor cells without HBx expression had no positive band. The result of TUNEL assay showed that there were less apoptotic cells in tumor tissues expressing HBx than that in control group cells. It was concluded that HBx could up-regulate the expression of survivin in hepatic carcinoma cells, which can inhibit apoptosis of hepatic carcinoma cells induced by adriamycin.


Assuntos
Animais , Feminino , Humanos , Camundongos , Antígenos de Neoplasias , Genética , Apoptose , Carcinoma Hepatocelular , Patologia , Virologia , Linhagem Celular Tumoral , Proteínas Inibidoras de Apoptose , Neoplasias Hepáticas , Patologia , Virologia , Camundongos Endogâmicos BALB C , Camundongos Nus , Proteínas Associadas aos Microtúbulos , Genética , Proteínas de Neoplasias , Transplante de Neoplasias , Transativadores , Genética , Transfecção , Regulação para Cima
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