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ABSTRACT: INTRODUCTION: Peutz-Jeghers syndrome is a rare autosomal dominantly inherited disease characterized by mucocutaneous pigmentations and gastrointestinal polyps. The polyps are located predominantly in the small intestine and usually cause intussusceptions. Adult intussusception caused by Peutz-Jeghers syndrome occurs very rarely. The purpose of this study was to analyze the clinical characteristics, preoperative diagnosis, and surgical management of Peutz-Jeghers syndrome associated with acute intussusception in adult patients. DISCUSSION: Consecutive patients with the postoperative diagnosis of acute intussusception caused by Peutz-Jeghers syndrome from 1995 to 2010 were reviewed retrospectively for this study. Data concerning clinical considerations, morphological examinations, and surgical procedure were analyzed. Different clinical manifestations were presented in patients with intussusception due to Peutz-Jeghers syndrome. Computed tomography associated or not with ultrasonography may be the most accurate examination for acute intussusceptions caused by Peutz-Jeghers syndrome. Surgical intervention is the first choice regimen in acute intussusceptions caused by Peutz-Jeghers syndrome. Prophylaxis and polypectomy of the entire small bowel is a worthy way in Peutz-Jeghers syndrome patients to reduce the frequency of laparotomies.
Journal of Gastrointestinal Surgery 12/2011; 15(12):2218-25. · 2.83 Impact Factor
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ABSTRACT: To investigate the influence of trauma on the tumorigenicity of rat glial tumor stem cells (C6-side population cell, C6-SP) in vivo.
Rat glial tumor stem cells C6-SP were isolated by flowcytometry. The biological behavior of C6-SP cells were observed by means of MTT experiment, single cell cloning, and cell cycle study with FCM CD133 expression was measured by immunofluorescence and FCM.. The tumorigenicity of C6-SP cells in vivo was evaluated by in situ tumor growth after intracranial implantation. The rat model was established by intracranial implantation of C6-SP cells. 10 days later, the rats in experimental groups were subjected to orthotopic or ectopic trauma. 24 days later, brain specimen was retrieved, gross tumor volume was measured, and Ki67 was evaluated by immunochemistry. The migration of stem cell was studied by the method to observe the relocation of C6-SP cells.
Clustrus tumor growth was seen when C6-SP cell was cultured in serum-free medium. The doubling time of C6-SP cell was shorter than ordinary C6 cell. Single stem cell cloning efficiency of C6-SP cell was 77% whereas that of ordinary C6 cell was 16.4%. Among cloned C6-SP cell and ordinary C6 cell, 49.7% +/- 5.2% and 35.2 +/- 4.3% were at G0/G1 phase respectively. CD133 expression of C6-SP cells was positively shown by immunofluorescence. Tumorigenesis was 100% 2 weeks after in situ implantation of C6-SP cells. Gross tumor volume and Ki67 expression of orthotopic trauma group were larger and higher than those of ectopic trauma group or blank control group (P < 0.05) whereas difference was insignificant in the later two groups (P > 0.05). Red stained cells relocation was seen in both traumatized groups and absent in controls.
C6-SP cells are the tumor stem cells (TSCs) for rat glioma. Trauma at the lesional site could increase tumorigenicity of the C6-SP cells. Moreover, trauma could induce migration of C6-SP cells in brain.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 03/2011; 42(2):161-5, 169.
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Kai Li,
Jie Zhang,
Jing-Jing Ren,
Qi Wang,
Kai-Yong Yang,
Zhu-Juan Xiong,
Yong-Qiu Mao,
Yan-Yu Qi,
Xiao-Wei Chen,
Feng Lan, Xiu-Jie Wang,
Heng-Yi Xiao,
Ping Lin,
Yu-Quan Wei
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ABSTRACT: Zinc finger proteins have been implicated as transcription factors in the differentiation and development of cells and tissues in higher organisms. The classical C2H2 zinc finger motif is one main type of motif of zinc finger proteins. Our previous studies have shown that Zfp637, which comprises six consecutively typical and one atypical C2H2 zinc finger motifs, is highly expressed in undifferentiated or poorly differentiated cell lines, but is moderately or slightly expressed in normal tissues. We have also demonstrated that Zfp637 can promote cell proliferation. However, its role in the regulation of cell differentiation remains unknown. We report here that endogenous Zfp637 as well as mTERT is expressed in proliferating C2C12 myoblasts and that their expression is downregulated during myogenic differentiation. Constitutive expression of Zfp637 in C2C12 myoblasts increased mTERT expression and telomerase activity, and promoted the progression of the cell cycle and cell proliferation. By contrast, endogenous repression of Zfp637 expression by RNA interference downregulated the mTERT gene and the activity of telomerase, and markedly reduced cell proliferation. Overexpression of Zfp637 also inhibited the expression of myogenic differentiation-specific genes such as MyoD and myogenin, and prevented C2C12 myoblast differentiation. Our results suggest that Zfp637 inhibits muscle differentiation through a defect in the cell cycle exit by potentially regulating mTERT expression in C2C12 myoblasts. This may provide a new research line for studying muscle differentiation.
Journal of Cellular Biochemistry 03/2010; 110(2):352-62. · 2.87 Impact Factor
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ABSTRACT: To construct the eukaryotic expression plasmid and establish stably transfected cell line, which contained the code gene of zinc finger protein637 (Zfp637), and to observe the effect of Zfp637 gene to the proliferation of tumor cells.
The Zfp637 DNA was amplified from the template of normal spleen tissue cDNA and cloned into the eukaryotic expression vector pEGFP-C3. The recombinant plasmid, named as pEGFP-Zfp637, was determined by restriction enzyme and sequencing analyses. Next the pEGFP-Zfp637 recombinant plasmid was transferred into mouse breast carcinoma EMT6 cells with lipofectamine 2000, and the stably transfected cells were selected by G418 (named Zfp637-EMT6). The growth condition of cells was observed, and subcellular localization of Zfp637 gene was located by fluorescence microscope at the same time. The Zfp637 mRNA expression in the transfected cells was detected by RT-PCR, and the proliferation of such cells was measured by MTT.
The analysis confirmed that the recombinant pEGFP-Zfp637 contained the Zfp637 full-length cDNA. The Zfp637 mRNA was over-expressed stably in Zfp637-EMT6. The growth of Zfp637-EMT6 was increased obviously when compared with the negative control group and blank group.
The recombinant pEGFP-Zfp637 has been constructed successfully, and the expression of the Zfp637 gene can promote the proliferation of cells. This recombinant eukaryotic expression plasmid can be used in advanced studies in the biological effects of Zfp637 and anti-tumor gene therapy.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 07/2009; 40(4):575-8, 603.
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ABSTRACT: The Na+/K+ ATPase B1 (ATP1B1) subunit gene is highly expressed in well-differentiated tumor cells, while it is hypoexpressed in poorly differentiated tumor cells. The expression of ATP1B1 is closely related to cell tight junction and polarity of epithelial cells. This study was to investigate the effect of specific interference of human Na+/K+ ATP1B1 using shRNA on cell proliferation and migration of gastric adenocarcinoma cell line SGC-7901.
Four shRNA plasmids specifically targeting different fragments of ATP1B1, sh150, sh295, sh562, sh765, were constructed and transiently transfected into SGC-7901 cells. Stable positive clones, shATP1B1-7901 cells, were sorted out by G418. The expression of ATP1B1 mRNA was detected by semi-quantitative RT-PCR and real-time PCR. Cell proliferation was measured by MTT, cell cycle distribution was assessed by flow cytometry, and clone forming was analyzed by the colony formation assay. Cellular migration was observed using the Transwell experiment.
At 24 h after transfection, the inhibition ratios of sh150, sh295, sh562, sh765 on ATP1B1 mRNA were (60.87+/-4.38)%, (44.93+/-2.24)%, (52.17+/-2.60)% and (52.17+/-2.60)% respectively in SGC-7901 cells, which were significantly higher than that of shNC control (3.00+/-0.15)%(p<0.05). Among the four ATP1B1 shRNAs, sh150 exerted the strongest effect (p<0.05) and was used in the following study. Assessed by RT-PCR and real-time PCR, the expression of ATP1B1 mRNA was inhibited by (85.72+/-5.22)% and (87.53+/-3.23)% in the shATP1B1-7901 group, in comparison with (3.3+/-0.22)% and (4.17+/-0.33)% in the shNC-7901 group (p<0.05). The proliferation ratio was higher in the shATP1B1-7901 group than in the shNC-7901 and SGC-7901 groups 3 days after transfection (p<0.05). Cells at S and G2/M phases in the shATP1B1-7901 group were significantly increased compared with those in the shNC-7901 and SGC-7901 groups (p<0.05). The clone formation rate of the shATP1B1-7901 group (68.50+/-2.65)% was higher than that of the shNC-7901 group (50.00+/-2.53)% and of the SGC-7901 group (52.50+/-2.11)% (p<0.05). Moreover, the migration ratio of the shATP1B1-7901 group(2.80+/-0.02)% was significantly enhanced comparing to the shNC-7901 (1.15+/-0.05)% and the shNC-7901 groups (1.25+/-0.02)% (p<0.05).
Silencing of ATP1B1 gene can enhance the proliferation and migration capability of SGC-7901 cells.
Ai zheng = Aizheng = Chinese journal of cancer 04/2009; 28(3):225-31.
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ABSTRACT: To investigate the effect of conjugated trienoic fatty acids on the growth inhibition, apoptosis in rat glioblastoma cells and to elucidate its mechanism of activity.
Rat glioblastoma cells were tested in vitro cytotoxicity, colony formation inhibition, Brdu incorporation after treatment with TCLA. Its effect of apoptosis induction was detected through Hoechst 33342 staining, cell cycle analysis. The expressions of ADPRTL1, CYP1A1 and PPAR-gamma genes were detected through RT-PCR.
After TCLA treatment, the proliferation of C6 cells were inhibited (40 micrommol/L, 72 h, viability 56.71% +/- 0.98%), this action acted as dose-time-dependent relations; colony formation decreased significantly (40 micrommol/L, 0) and BrdU labeling index of cancer cells decreased (63.1% +/- 1.0% vs 95.6 % +/- 1.4%); apoptotic cells increased; By FCM analysis, the apoptotic indices increased, the cells increased in G0/G1 phase, decreased in S phase, which have signigicant difference; RT-RCR showed that TCLA signigicantly increased the level of ADPRTL1, CYP1A1, and PPAR-gamma mRNA expression.
The findings in this experimental study suggested that TCLA has potent cytotoxicity and induction apoptosis in human and rat glioblastoma cells, its mechanism of activity might be associated with the inhibition of DNA synthesis, cell cycle arrest, up-regulation the expression of apoptosis related genes ADPRTL, CYP1A1, PPAR-gamma.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 08/2008; 39(4):570-4.
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Ping Lin,
Yan-Rong Lu,
Jie Zhang,
Yu-Quan Wei, Xiu-Jie Wang,
Sheng-Fu Li,
Qi Wang,
Zhu-Juan Xiong,
Qi-Zhi Ning,
Song Lei,
Yong-Qiu Mao,
Jing-Qiu Cheng
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ABSTRACT: Dendritic cells (DCs) are important cells in initiating an immune response. A generation of functional DCs has potential clinical use in treating cancer. However, the source of DCs and patient immunodeficiency with cancer have been hindrances in clinical therapy. We generated DCs from human umbilical cord blood mononuclear cells (UBMCs) with recombinant human granulocyte-macrophage colony stimulating factor, recombinant human interleukin-4, and recombinant human tumor necrosis factor-alpha. The mature DC-A549 lung cancer vaccine (AgL-DC) was prepared through loading A549 lysate, treating with lipopolysaccharide (LPS) and positive selecting with CD83 magnetic beads. AgL-DC can secrete interleukin (IL)-12 and IL-1. Further in vitro analysis showed that AgL-DC notably induced human UBMC lymphocyte proliferation (p < 0.01) by 3-(4,5-dimethylthiazol-z-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, increased the cytotoxic T-lymphocyte (CTL) activity of UBMC lymphocytes against A549 cells (p < 0.05, at effector cells:target cells ratios of 50:1 and 100:1) by lactate dehydrogenase (LDH) cytotoxic assay, and improved production of IL-6 and tumor necrosis factor-beta (p < 0.01, p < 0.05) by enzyme-linked immunosorbent assay. Subsequently, the reconstitute immunity model in severe combined immunodeficiencies (SCID) mice has been established using human UBMC transplantation, and similar trends to results of UBMC in vitro experiments have been shown in lymphocyte proliferation, CTL activity, and IL-6 and tumor necrosis factor-beta secretion levels in these models. AgL-DC also significantly (p < 0.01) increased the antitumor effect in vivo. The tumor infiltrating immunocytes were positively expressed human CD83 and CD3 molecules, and they were negatively expressed in tumor tissue treated with control. These results have demonstrated that umbilical cord DCs are a useful source of vaccine cells for augmenting CTL-mediated cytotoxicity and have potential usefulness in cellular therapy for human cancer in a new vaccination strategy.
Cancer Biotherapy & Radiopharmaceuticals 07/2008; 23(3):321-31. · 1.44 Impact Factor
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Yan-rong Lu,
Yu Yuan, Xiu-jie Wang,
Ling-ling Wei,
You-nan Chen,
Cong Cong,
Sheng-fu Li,
Dan Long,
Wei-dong Tan,
Ying-qiu Mao,
Jie Zhang,
You-ping Li,
Jing-qiu Cheng
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ABSTRACT: Mesenchymal stem cells (MSCs) play an important role in the development and growth of tumor cells. The purpose of this study is to confirm the effect of MSCs on tumor cell growth in vitro and in vivo and to elucidate the mechanism. MSCs were isolated from mouse bone marrow and cocultured with murine hepatoma H22, lymphoma (YAC-1 and EL-4) and rat insulinoma INS-1 cell lines. The growth inhibitory effect of MSCs on tumor cells was tested through MTT and 3H-TdR incorporation assay. The apoptosis induction effect of MSCs on tumor cells was assessed with flow cytometry (FCM) and RT-PCR assay. MSCs were inoculated into BALB/c mice alone or coinoculated with ascitogenous hepatoma cells intraperitonealy, respectively. The tumor growth inhibition of MSCs was investigaed through the incidence and volume of ascites formation, and the immunosuppression effect was studied with splenocyte response to ConA stimulation test and T cell subsets analysis (FCM). The results showed that MSCs exhibited a number-dependent growth inhibitory effect on murine tumor cell lines in vitro and inhibited the growth of ascitogenous hepatoma cells in vivo without host immunosuppression. MSCs could upregulate tumor cells mRNA expression of cell cycle negative regulator p21 and apoptosis associated protease caspase 3. The findings of this experimental study demonstrated that MSCs had potential inhibitory effects on tumor cell growth in vitro and in vivo without host immunosuppression, by inducing apoptotic cell death and G(0)/G(1) phase arrest of cancer cells.
Cancer biology & therapy 03/2008; 7(2):245-51. · 2.64 Impact Factor
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ABSTRACT: To investigate the effect of SOCS1 expression inhibition on hepatocellular carcinoma-dendritic cell vaccine stimulated by LIGHT.
The dendritic cells (DC) were generated from mouse bone marrow (BMDC) by cultured in medium containing rmGM-CSF and rmIL-4. The vaccine cells were prepared by loaded with hepatocellular carcinoma HepA antigen and further treated with or without LIGHT and SOCS1 antisense oligonucleotide (AS1). For detecting the maturity of the vaccine cells, the expression of the cell's surface molecules CD40 and CD86 were measured by FACS, and IL-12 and IL-1 secretion from the cells were determined by ELISA. And the CTL activity, cellular proliferation, IL-6 and TNF-beta secretion levels of the vaccine-stimulated lymphocytes were also assessed for analyzing the immune response of lymphocyte.
CD40 and CD86 expression of the prepared vaccine cells were obviously enhanced by treatment of LIGHT and AS1, and so were IL-12 and IL-1 (P<0.01). It was also observed that CTL activity, cellular proliferation and IL-6 and TNF-beta secreting levels of lymphocytes that were stimulated by the vaccine cells treated with AS1 were notably enhanced.
Inhibiting SOCS1 can improve the maturation of hepatocellular carcinoma-DC vaccine cell and can increase its inducing ability of anti-cancer immune response.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 03/2008; 39(2):177-80.
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ABSTRACT: To establish the eukaryotic expression plasmid containing the code gene of Na+, K+-ATPase beta1-subunit (ATP1B1) and the basis of ATP1B1 applied to antitumor gene therapy.
The ATP1B1 cDNA was amplified from leukocyte gene library and then cloned into the eukaryotic expression vector pEGFP-C3. The recombinant plasmid, named as pEGFP-ATP1B1, was determined with restriction enzyme and sequencing analyses. Next pEGFP-ATP1B1 was transferred into gastric adenocarcinoma SGC-7901 cells by lipofectamine, then ATP1B1 mRNA expression in transfected cells was detected by real-time PCR, and also ATPase was detected after cell transfection, as well as the proliferation of such cells was measured by MTT.
The analysis confirmed that the recombinant pEGFP-ATP1B1 contained the ATP1B1 cDNA. After cell transfection, the expression of ATP1B1 mRNA(129.2%) and the activity of ATPase [(2.95+/-0.210)%] were higher, and the growth of the SGC-7901 cells transfected with ATP1B1 was inhibited obviously when compared with the control group.
The recombinant pEGFP-ATP1B1 is constructed successfully, and this recombinant eukaryotic expression vector could be used in additional studies on the biological effect of ATP1B1 and its use in anti-tumor gene therapy.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 03/2008; 39(2):169-72, 176.
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ABSTRACT: To detect the relation between the member LIGHT of TNF superfamily and the suppressor of cytokine signaling 3 (SOCS3), and to investigate the effect of SOCS3 on dendritic cell (DC) maturation induced by LIGHT.
Bone marrow-derived DC (BMDC) was generated from mouse bone marrow monocyte by culturing with rmGM-CSF, rmIL-4 in vitro. SOCS3 mRNA in BMDC was analyzed by RT-PCR, and the protein of SOCS3 was measured by Western blot. After blocking the SOCS3 expression with the specific anti-sense oligonucleotide, we applied the flow cytometry to measure the expression of CD86 and CD40 on DC for making clear whether the silence of SOCS3 would regulate the LIGHT-stimulated DC maturation.
With the effect of LIGHT, the level of SOCS3 mRNA and protein in BMDC sharply increased. The specific antisense oligonucleotide could effectively block SOCS3 mRNA expressing in BMDC with the ratio of 49% and block SOCS3 protein expression with the ratio of 45%. Compared with SOCS3-unblocked DC, the SOCS3-blocked BMDC with stimulation of LIGHT showed higher CD40 and CD86 (P < 0.05).
LIGHT enhances the expression of SOCS3 during stimulating BMDC maturation. As more sensitive to LIGHT, the SOCS3-blocked BMDC is driven to more mature. SOCS3 presents a negative regulation mechanism in BMDC maturation induced
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 07/2007; 38(4):644-8.
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ABSTRACT: To investigate the growth inhibition and multidrug resistance (MDR) reversing effect of tanshinone I A on human breast cancer cells with estrogen receptor (ER) negative, and to elucidate its mechanism of activity.
Human ER negative breast cancer cells (MDA-MB-231) were tested in vitro for cytotoxicity and colony formation inhibition. Brdu incorporation and cell cycle distribution were also checked through flow cytometry (FCM). With RT-PCR, the expressions of ADP-ribosyltransferase CNAD+; poly (ADP-ribose) polymerase)-like 1 (ADPRTL1), cytochrome P450 subfamily I (CYP1A1) and breast cancer resistance protein (BCRP/ABCG2) mRNA were detected for testing the response to tanshinone 1 A treatment.
After tanshinone I A treatment, the proliferation, colony formation and Brdu labeling indices of cancer cells decreased (P<0. 05). By FCM analysis, the increase of subG, and G0/G1 phase cell populations and decrease of S and G2/M phase cells were observed (P<O. 01), both ADPRTL1 and CYP1A1 mRNA expression increased (P< 0. 05), while BCRP/ABCG2 mRNA expression was decreasing (P<0. 05).
The findings in these studies suggest that tanshinone I A exhibits the potent cytotoxicity and MDR reversing potential to human ER negative breast cancer cells. The mechanism for such effects may be associated with the inhibition of DNA synthesis, induction of apoptosis, cell cycle arrest and up-regulation of ADPRTL1, CYP1A1, and down-regulation of BCRP/ABCG2 expression in cancer cells.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 06/2007; 38(3):391-5.
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ABSTRACT: To investigate the damaging effect of high-intensity focused ultrasound (HIFU) on cancer cells and the inhibitory effect on tumor growth.
Murine H22 hepatic cancer cells were treated with HIFU at the same intensity for different lengths of time and at different intensities for the same length of time in vitro, the dead cancer cells were determined by trypan blue staining. Two groups of cancer cells treated with HIFU at the lowest and highest intensity were inoculated into mice. Tumor masses were removed and weighed after 2 wk, tumor growth in each group was confirmed pathologically.
The death rate of cancer cells treated with HIFU at 1 000 W/cm2 for 0.5, 1, 2, 4, 8, and 12 s was 3.11+/-1.21%, 13.37+/-2.56%, 38.84+/-3.68%, 47.22+/-5.76%, 87.55+/-7.32%, and 94.33+/-8.11%, respectively. A positive relationship between the death rates of cancer cells and the length of HIFU treatment time was found (r = 0.96, P<0.01). The death rate of cancer cells treated with HIFU at the intensity of 100, 200, 400, 600, 800, and 1 000 W/cm2 for 8 s was 26.31+/-3.26%, 31.00+/-3.87%, 41.97+/-5.86%, 72.23+/-8.12%, 94.90+/-8.67%, and 99.30+/-9.18%, respectively. A positive relationship between the death rates of cancer cells and the intensities of HIFU treatment was confirmed (r = 0.98, P<0.01). The cancer cells treated with HIFU at 1 000 W/cm2 for 8 s were inoculated into mice ex vivo. The tumor inhibitory rate was 90.35% compared to the control (P<0.01). In the experimental group inoculated with the cancer cells treated with HIFU at 1 000 W/cm2 for 0.5 s, the tumor inhibitory rate was 22.9% (P<0.01). By pathological examination, tumor growth was confirmed in 8 out of 14 mice (57.14%, 8/14) inoculated with the cancer cells treated with HIFU at 1 000 W/cm2 for 8 s, which was significantly lower than that in the control (100%, 15/15, P<0.05).
HIFU is effective on killing or damage of H22 hepatic cancer cells in vitro and on inhibiting tumor growth in mice ex vivo.
World Journal of Gastroenterology 07/2005; 11(28):4317-20. · 2.47 Impact Factor
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ABSTRACT: To investigate the effect of tanshinone IIA on HL-60 and K562 cells apoptosis, and to assay the inhibition of the telomerase activities in the leukemia cell apoptosis induced by Tanshinone.
Using the techniques of cell culture in vitro, flow cytometry and PCR-TRAP observed the telomerase activities and apoptosis of HL-60 and K562 cells which treated by Tan IIA.
0.5 microg x mL(-1) Tan IIA could obviously inhibit HL-60 and K562 cell lines growth (P < 0.05), down-regulate c-myc, bcl-2 gene and up-regulate c-fos and p53 gene expression as well as induce leukemia cell apoptosis, the apoptotic rates of HL-60 and K562 cells were 11.8% and 21.8% respectively. The telomerase activities significant decreased, the inhibiting rates in HL60 and K562 cells were 30.8% and 50.8% respectively.
Tan IIA could significantly inhibit the proliferation and telomerase activities of HL-60 and K562 cells and induce the leukemia cell apoptosis.
Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica 02/2005; 30(3):207-11.
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ABSTRACT: To investigate the potential involvement of leptin in carcinogenesis of hepatocellular carcinoma (HCC) and to elucidate the etiology, carcinogenesis and progress of HCC.
Expressions of Ob gene product, leptin and its receptor, Ob-R were investigated in 36 cases of HCC specimens and corresponding adjacent non-tumorous liver tissues with immunohistochemical staining. The effect of leptin on proliferation of Chang liver cell line and liver cancer cell line SMMC-7721 was studied with cell proliferation assay (MTT).
Leptin expression was detected in 36 cases of adjacent non-tumorous liver tissues (36/36, 100%) with moderate (++) to strong (+++) intensity; and in 72.22%(26/36) of HCC with weaker (+) intensity (P<0.05). Thirty of 36 (83.33%) cases of adjacent non-tumorous liver tissues were positive for Ob-R, with moderate (++) to strong (+++) intensity. In HCC, 11/36 (30.56%) cases were positive, with weak (+) intensity (P<0.05). In cell proliferation assay, leptin inhibited the proliferation of Chang liver cells. The cell survival rate was 10-13% lower than that of the untreated cells (P>0.05). Leptin had little effect on the proliferation of liver cancer cells (P>0.05).
High level expression and decreased or absent expression of leptin and its receptor in adjacent non-tumorous liver cells and HCC cells, inhibitory effect of leptin on the proliferation of normal Chang liver cells and no effect of leptin on proliferation of liver cancer cells, may provide new insights into the carcinogenesis and progression of human HCC. It could be assumed that leptin acting as an inhibitor and/or promoter, is involved in the process of carcinogenesis and progress of human HCC.
World Journal of Gastroenterology 09/2004; 10(17):2478-81. · 2.47 Impact Factor
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ABSTRACT: To evaluate the effects of tanshinone II-A on inducing growth inhibition and apoptosis of human hepatocellular carcinoma (HCC) cells.
The human hepatocellular carcinoma cell line SMMC-7721 was used for the study. The cells were treated with tanshinone II-A at different doses and different times. Cell growth and proliferation were measured by MTT assay, cell count and colony-forming assay. Apoptosis induction was detected by microscopy, DNA ladder electrophoresis and flow cytometry.
In MTT assay, the inhibitory effect became gradually stronger with the passage of time, 24, 48, 72 and 96 h after treatment with tanshinone II-A, and the most significant effect was observed at 72 h. On the other hand, the increase of doses (0.125, 0.25, 0.5, 1.0 mg/L tanshinone II-A) resulted in enhanced inhibitory effect. The growth and proliferation of SMMC-7721 cells were obviously suppressed in a dose- and time-dependent manner. The results of cell count were similar to that of MTT assay. In colony-forming assay, the colony-forming rates were obviously inhibited by tanshinone II-A. In tanshinone II-A group, the morphology of cellular growth inhibition and characteristics of apoptosis such as chromatin condensation, crescent formation, margination and apoptotic body were observed under light and transmission electron microscopes. DNA ladder of cells was presented in electrophoresis. The apoptosis index (AI) was 16.9% (the control group was 4.6%) in flow cytometry. The cells were arrested in G(0)/G(1) phase, and the expressions of apoptosis-related genes bcl-2 and c-myc were down-regulated and fas, bax, p53 up-regulated.
Tanshinone II-A could inhibit the growth and proliferation of HCC cell effectively in vitro by apoptosis induction, which was associated with up-regulation of fas, p53, bax, expression and down-regulation of bcl-2 and c-myc.
World Journal of Gastroenterology 08/2004; 10(14):2024-8. · 2.47 Impact Factor
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ABSTRACT: Tanshinone IIA is a derivative of phenanthrene-quinone isolated from Salvia miltiorrhiza BUNGE, which is a traditional herbal medicine that is used to treat cardiovascular diseases. Recent studies showed that Tanshinone IIA possesses cytotoxic activity against many kinds of human carcinoma cell lines, induces differentiation and apoptosis and inhibits invasion and metastasis of cancer cells. Its mechanisms are thought as inhibiting DNA synthesis and proliferation of cancer cells, regulating the expression of genes related to proliferation, differentiation, and apoptosis, inhibiting the telomerase activity of cancer cells, and changing the expression of cellular surface antigen.
Ai zheng = Aizheng = Chinese journal of cancer 01/2004; 22(12):1363-6.
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Xiu-jie Wang,
Shu-ian Yuan,
Jie Zhang,
Yan-rong Lu,
Yan-ping Wang,
Xiao-he Chen,
Qi-zhi Ning,
Yu-rui Fu,
Bo-tao Liu,
Wen-fu Zeng,
Yue-ming He
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ABSTRACT: To investigate the killing effect of high intensity focused ultrasound (HIFU) on human tumor cells and study the mechanism of its action.
Human breast cancer cells MCF-7 were treated with different intensity of HIFU in vitro and incubated. The killing effect and proliferation inhibition effect of HIFU on tumor cells were investigated with the methods of trypan blue exclusion assay, MTT assay and colony formation assay. And the cell cycle, apoptotic cells and the expressions of P53, BCL-2, FAS and HSP70 were measured with flow cytometry.
After HIFU treatment, the death rates of cancer cell increased, the proliferation of cell waned (P < 0.05), the number of colony formation decreased (P < 0.001), the cell number increased in G0/G1 phase (P < 0.05) and decreased in S phase, the apoptotic indices increased (P < 0.01), the expression of HSP70 was enhanced, and no significant changes of P53, BCL-2, FAS expressions were found (P > 0.05).
HIFU produces significant effects such as killing, proliferation inhibition and colony formation inhibition on human breast cancer cells; its mechanism of action may be associated with the inhibition of DNA synthesis. In addition, HIFU treatment can induce apoptotic cell death, which may not be associated with the mediation and regulation of P53, BCL-2 and FAS genes.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 01/2004; 35(1):60-3.
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World Journal of Gastroenterology 11/2000; 6(5):750-753. · 2.47 Impact Factor
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ABSTRACT: AIM:To investigate the activation, expression of c-src gene and its role in the carcinogenetic process of human cardia adenocarcinoma (CA).METHODS:Fifty six cases of CA, 34 cases of normal, 36 cases of protiferative epithelia adjacent to carcinoma, and 20 cases of lymph node metastases of CA were studied for PP60(c-src),the expression product of c-src gene immunohistochemically by using the specific monoclonal antibody,Mab327.RESULTS: The positive rates of PP60(c-src) in the normal epithelia,protiferative epithelia, CA and lymph node metastases were 29.4% (10/34), 94.4% (34/36), 71.4% (40/56) and 60.0%(12/20), respectively, among them, the differences of the positive rates were statistically significant (P < 0.01). The expression levels of PP60(c-src) in CA and proli ferative epithelia were significantly higher than that in the normal epithelia(P< 0.01).The PP60(c-src) positive rates in the papillary, tubular, poorly different-tiated and mucous adenocarcinoma were 75.0% (6/8), 81.8% (18/22), 50.0% (10/20) and 100.0% (6/6), respectively, whereas those of tubular and mucous adenocarcinomas were significantly higher than those of papillary and poorly differentiated adenocar-cinomas (P < 0.05), and the PP60(c-src) expression levels of tubular and mucous adenocarcinomas were also significantly higher than those of papillary and poorly differentiated adenocarcinomas (P< 0.01).CONCLUSION:The activation and expression of c-src gene are associated with the initiation and development of human CA; the protein amount of PP60(c-src)increased during the process of carcinogenesis; and PP60(c-src) expression is also related to lymph node metastases.
World Journal of Gastroenterology 12/1999; 5(6):488-491. · 2.47 Impact Factor
