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Li-Xin Sun,
Zhi-Bin Lin,
Xin-Suo Duan,
Jie Lu,
Zhi-Hua Ge,
Min Li,
En-Hong Xing,
Tian-Fei Lan,
Miao-Miao Jiang,
Ning Yang,
Wei-Dong Li
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ABSTRACT: Immune responses to tumor-associated antigens are often detectable in tumor-bearing hosts, but they fail to eliminate malignant cells or prevent development of metastases. Tumor cells produce factors such as interleukin-10, transforming growth factor-β1 and vascular endothelial growth factor (VEGF) that suppress the function of immune cells or induce apoptosis of immune cells. Culture supernatant of tumor cells may contain these immunosuppressive factors which suppress lymphocyte activation. CD71 and FasL are two important molecules that are expressed upon lymphocyte activation. Counteraction against suppression CD71 and FasL expression upon lymphocyte activation may benefit tumor control. A potential component with this effect is Ganoderma lucidum polysaccharides (Gl-PS). In this study, Gl-PS was used on lymphocytes incubating with culture supernatant of B16F10 melanoma cells (B16F10-CS) in the presence of phytohemagglutinin. Following induction with phytohemagglutinin, B16F10-CS suppressed CD71 expression in lymphocytes (as detected by immunofluorescence and flow cytometry), proliferation in lymphocytes (as detected by MTT assay), and FasL expression in lymphocytes (as detected by immunocytochemistry and western blot analysis), while Gl-PS fully or partially counteracted these suppressions. Gl-PS showed counteractive effects against suppression induced by B16F10-CS on CD71 and FasL expression upon lymphocyte activation, suggesting the potential of Gl-PS to facilitate cancer immunotherapy.
Experimental and therapeutic medicine 04/2013; 5(4):1117-1122.
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ABSTRACT: Melanoma is one of the most deadly skin cancers. T-cadherin is an atypical member of the cadherin superfamily as it lacks the transmembrane and cytoplasmic domains and is anchored to cell membranes through glycosylphosphatidylinositol (GPI) anchors. T-cadherin downregulation is associated with a poorer prognosis in various carcinomas, such as lung, ovarian, cervical and prostate cancer, while in the majority of cancer cell lines, T-cadherin re-expression inhibits cell proliferation and invasiveness, increases susceptibility in apoptosis and reduces tumor growth in in vivo models. The functional relevance of T-cadherin gene expression in melanoma progression remains to be clarified. The present study was designed for this purpose. The T-cadherin gene was transfected into B16F10 melanoma cells to express T-cadherin in the cells which were originally deficient in T-cadherin expression. The proliferation, invasiveness, apoptosis and cell cycle of the transfected B16F10 melanoma cells were analyzed. The present study showed that the expression of T-cadherin in B16F10 melanoma cells markedly reduced cell proliferation and permeation through Matrigel-coated membranes, representing invasiveness. The percentage of early apoptotic cells and cells in the G2/M phase of the cell cycle was markedly increased compared with either parental B16F10 (without transfection) or empty pEGFP-N1 (without T-cadherin gene)-transfected B16F10 cells, suggesting G2/M arrest, with similarity between the parental and empty pEGFP-N1-transfected B16F10 cells. T-cadherin is important in melanoma progression and may be a possible target for therapy in melanoma and certain other types of cancer.
Oncology letters 04/2013; 5(4):1205-1210. · 0.11 Impact Factor
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Jie Lu, Li-Xin Sun,
Zhi-Bin Lin,
Xin-Suo Duan,
Zhi-Hua Ge,
En-Hong Xing,
Tian-Fei Lan,
Ning Yang,
Xue-Jun Li,
Min Li,
Wei-Dong Li
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ABSTRACT: It is well-documented that macrophages have the functions to regulate antitumor immune response. Antitumor response can be launched by a series of events, starting with inflammation mediated by monocyte/macrophages, which stimulates natural killer and dendritic cells and finally activates the cytotoxic lymphoid system. Monocytes/macrophages may be the first line of defense in tumors. However, specific and nonspecific immunotherapy for human cancer has shown no success or limited success in clinical trials. Part of the reasons attribute to tumor-derived soluble factors that suppress functions of immune cells or induce apoptosis of these cells, including macrophages. Therefore, antagonism of the suppression on the macrophages is an important goal for tumor immunotherapy. To achieve this purpose, Ganoderma lucidum polysaccharides (Gl-PS) with multiple bioactivities were used on mouse peritoneal macrophages incubating with culture supernatants of B16F10 melanoma cells (B16F10-CS). It was shown that the viability, phagocytic activity, NO production, TNF-α production and activity in peritoneal macrophages after activation by lipopolysaccharide were suppressed by B16F10-CS, while the suppressions were fully or partially antagonized by Gl-PS. In conclusion, B16F10-CS is suppressive to the viability, phagocytic activity, NO production, TNF-α production and activity in peritoneal macrophages while Gl-PS had the antagonistic effects against this suppression, suggesting this potential of Gl-PS to facilitate cancer immunotherapy. Copyright © 2013 John Wiley & Sons, Ltd.
Phytotherapy Research 03/2013; · 2.09 Impact Factor
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Li-Xin Sun,
Zhi-Bin Lin,
Xin-Suo Duan,
Jie Lu,
Zhi-Hua Ge,
Xue-Fei Li,
Xue-Jun Li,
Min Li,
En-Hong Xing,
You-Xin Song,
Jing Jia,
Wei-Dong Li
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ABSTRACT: It is obvious that malignant cells evade from immune system in patients with manifest malignancy. Deficient major histocompatibility complex (MHC) class I and costimulatory molecules on malignant cells partially consist of evasion strategy since antigen bond MHC and costimulatory molecules provide two signals necessary for T cell activation. Therefore, enhancement of MHC-I and costimulatory molecules may favor restraint of the evasion. For this purpose, Ganoderma lucidum Polysaccharides (Gl-PS) was used on B16F10 melanoma cells in this study.
Immunocytochemistry and flowcytometry were used to determine the H-2K(b) and H-2D(b) (two prominent MHC class I molecules in C57BL mouse) as well as B7-1 and B7-2 (two prominent costimulatory molecules) expression on B16F10 cells after incubation with Gl-PS, while messenger ribonucleic acid (mRNA) of these molecules was detected by reverse transcription polymerase chain reaction (RT-PCR).
The H-2K(b) and H-2D(b), and B7-1 and B7-2 on B16F10 cells and mRNAs of these molecules were enhanced by Gl-PS, and more efficient antitumor cytotoxicity was induced by the Gl-PS treated cells.
The MHC class I molecules and costimulatory molecules may be enhanced by Gl-PS, and more efficient immune cell mediated cytotoxicity against these B16F10 cells may be induced, which may favor cancer therapy.
Journal of Drug Targeting 06/2012; 20(7):582-92. · 2.70 Impact Factor
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ABSTRACT: ObjectiveTo investigate the effect of co-culture between colon cancer cells (SW1116) and human liver sinusoidal endothelial cells (HLSECs)
on cancer cell metastasis, and to provide a novel model for studying the mechanism of colon cancer liver metastasis.
MethodsHLSECs and SW1116 were co-cultured for 21 rounds in vitro. Transwell migration, gelatin-zymography, CCK-8 proliferation and
colony formation assays were used to examine the invasion, proliferation, and colony forming ability of cancer cells. Assays
were carried out to examine tumor growth ability and liver metastasis. The associated molecular change was examined by western
blotting.
ResultsAfter 21 selection rounds, colon cancer cells SW1116P21 displayed a clear boundary. Compared with the SW1116 cells, SW1116P21
cells had a greater invasive ability, cell proliferation and colony formation in soft agar. A gelatin-zymography assay showed
that the ability of SW1116P21 cells to secrete matrix metalloproteinase-2/9 was significantly greater than that of SW1116
cells. Additionally, the capacity for subcutaneous tumor formation of SW1116P21 was significantly increased. It was found
that mice injected with SW1116P21 cells developed significantly more visually observable liver nodules than mice injected
with SW1116 cells. Western blotting showed increased vimentin expression and decreased E-cadherin expression in the SW1116P21
cells, compared with the SW1116 cells.
ConclusionThe interaction between SW1116 and HLSECs may promote tumor cell invasion, proliferation and colony formation in vitro, and
tumor formation and liver metastasis in vivo. An epithelial-mesenchymal transition occurs in SW1116P21 cells, which contributes
to the change in the characteristics of tumor cells.
Key Wordscolon cancer–human liver sinusoidal endothelial cells–co-culture–liver metastasis
Clinical Oncology and Cancer Research 05/2012; 8(3):138-143.
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ABSTRACT: Pristimerin isolated from Celastrus and Maytenus spp can inhibit proteasome activity. However, whether pristimerin can modulate cancer metastasis is unknown.
The impacts of pristimerin on the purified and intracellular chymotrypsin proteasomal activity, the levels of regulator of G protein signaling 4 (RGS 4) expression and breast cancer cell lamellipodia formation, and the migration and invasion were determined by enzymatic, Western blot, immunofluorescent, and transwell assays, respectively.
We found that pristimerin inhibited human chymotrypsin proteasomal activity in MDA-MB-231 cells in a dose-dependent manner. Pristimerin also inhibited breast cancer cell lamellipodia formation, migration, and invasion in vitro by up-regulating RGS4 expression. Thus, knockdown of RGS4 attenuated pristimerin-mediated inhibition of breast cancer cell migration and invasion. Furthermore, pristimerin inhibited growth and invasion of implanted breast tumors in mice.
Pristmerin inhibits proteasomal activity and increases the levels of RGS4, inhibiting the migration and invasion of breast cancer cells.
Asian Pacific journal of cancer prevention: APJCP 01/2012; 13(4):1097-104. · 0.66 Impact Factor
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ABSTRACT: Nogo-66 is a 66-amino-acid-residue extracellular domain of Nogo-A, which plays a key role in inhibition neurite outgrowth of central nervous system through binding to the Nogo-66 receptor (NgR) expressed on the neuron. Recent studies have confirmed that NgR is also expressed on the surface of macrophages/microglia in multiple sclerosis, but its biological effects remain unknown. In the present study, our results demonstrated that Nogo-66 triggered microglia anti-adhesion and inhibited their migration in vitro, which was mediated by NgR. We also assessed the roles of small GTP (glycosyl phosphatidylinositol)-binding proteins of the Rho family as the downstream signal transducers on the microglia adhesion and mobility induced by Nogo-66. The results showed that Nogo-66 activated RhoA and reduced the activity of Cdc42 in the meanwhile, which further triggered the anti-adhesion and migration inhibition effects to microglia. Nogo-66 inhibited microglia polarization and membrane protrusion formation, thus might eventually contribute to the decreasing capability of cell mobility. Taken together, the Nogo-66/NgR pathway may modulate neuroinflammation via mediating microglia adhesion and migration in addition to its role in neurons. Better understanding the relationship between Nogo-66/NgR and neuroinflammation may help targeting NgR for treating central nervous system diseases related with inflammation.
Journal of Neurochemistry 12/2011; 120(5):721-31. · 4.06 Impact Factor
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ABSTRACT: Restoration of epithelial continuity in the intestinal surface after extensive destruction is important since intestinal epithelial cells stand as a boundary between the body's internal and external environment. Polysaccharides from Ganoderma lucidum (Gl-PS) may benefit intestinal epithelial wound healing in different aspects, which awaits clarification. To identify potential effects, a non-transformed small-intestinal epithelial cell line, IEC-6 cells, was used.
Effects on epithelial cell proliferation, migration, morphology of differentiation and transforming growth factor beta (TGF-β) protein expression, as well as the cellular ornithine decarboxylase (ODC) mRNA and c-Myc mRNA expression, were assessed, respectively, by MTT assay, wound model in vitro, observation under a microscope after hematoxylin and eosin staining, enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction assays.
It was shown that Gl-PS stimulated IEC-6 cell proliferation and migration significantly in a dose-dependent manner; 10 µg/ml Gl-PS improved the morphology of differentiation in IEC-6 cells. Inefficacy in expression of TGF-β in IEC-6 cells indicated a possible TGF-β independent action of Gl-PS. However, Gl-PS increased ODC mRNA and c-Myc mRNA expression in a dose-dependent manner, indicating, at least partially possible involvement of ODC and c-Myc gene expression in improvement of intestinal wound healing.
These results suggest the potential usefulness of Gl-PS to cure intestinal disorders characterized by injury and ineffective repair of the intestinal mucosa.
The Journal of pharmacy and pharmacology. 12/2011; 63(12):1595-603.
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Li-Xin Sun,
Zhi-Bin Lin,
Xin-Suo Duan,
Jie Lu,
Zhi-Hua Ge,
Xue-Jun Li,
Min Li,
En-Hong Xing,
Jing Jia,
Tian-Fei Lan,
Wei-Dong Li
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ABSTRACT: Tumour cells produce factors such as interleukin 10 (IL-10), transforming growth factor β1 (TGF-β1) and vascular endothelial growth factor (VEGF) that suppress the function of immune cells or induce apoptosis of immune cells. One of the most important goals of tumour immunotherapy is to antagonize this suppression on immune cells. Ganoderma lucidum polysaccharides (Gl-PS) may have this potential. The purpose of this study was to determine the antagonistic effects of Gl-PS on the suppression induced by B16F10 melanoma cell culture supernatant (B16F10-CS) on lymphocytes.
Gl-PS was used on lymphocytes incubated with B16F10-CS. Enzyme-linked immunosorbent assay was used to determine the levels of IL-10, TGF-β1 and VEGF in B16F10-CS. The MTT assay was used to determine the proliferation of lymphocytes. Immunocytochemistry and Western blot assay were used to determine perforin and granzyme B production in lymphocytes.
There were elevated levels of IL-10, TGF-β1 and VEGF in B16F10-CS. The lymphocyte proliferation, and perforin and granzyme B production in lymphocytes after induction with phytohemagglutinin, as well as lymphocyte proliferation in the mixed lymphocyte reaction, were suppressed by B16F10-CS. This suppression was fully or partially antagonized by Gl-PS.
B16F10-CS suppressed lymphocyte proliferation and perforin and granzyme B production in lymphocytes after induction with phytohemagglutinin, as well as lymphocyte proliferation in the mixed lymphocyte reaction. This suppression may be associated with elevated levels of immunosuppressive IL-10, TGF-β1 and VEGF in B16F10-CS. Gl-PS had antagonistic effects on the immunosuppression induced by B16F10-CS, suggesting the potential for Gl-PS in cancer immunotherapy.
The Journal of pharmacy and pharmacology. 05/2011; 63(5):725-35.
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ABSTRACT: The immune system in patients with cancer often fails to control tumour growth because of deficient immunogenicity of tumour cells. Ganoderma lucidum polysaccharides (Gl-PS) are believed to have anti-tumour effects by boosting host immune function. Additionally, Gl-PS may have some direct effects on tumour cells in the activation of lymphocytes, thus enhancing the immunogenicity of tumour cells. We tested the effects of Gl-PS in lymphocyte activation by incubating Gl-PS with a tumour cell line deficient in antigen presentation. Our study showed that Gl-PS can promote B16F10 melanoma cells to induce lymphocyte proliferation, CD69 and FasL expression and IFN-γ production, indicating that Gl-PS can improve the nature of B16F10 cells to activate lymphocytes. Furthermore, H-2D(b) [a major histocompatibility (MHC) class I molecule], and B7-1 and B7-2 (two prominent co-stimulatory molecules expressed on B16F10 cells) were enhanced by Gl-PS, suggesting that these molecules may at least partially be involved in the process of Gl-PS on B16F10 cells to activate lymphocytes.
Basic & Clinical Pharmacology & Toxicology 10/2010; 108(3):149-54. · 2.18 Impact Factor
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ABSTRACT: To further explore the effect of annexin I on the tumor growth of human pancreatic cancer in nude mice.
To knock down the expression of annexin I in pancreatic carcinoma cells by RNAi. A nude mouse model of human pancreatic cancer was established by subcutaneous inoculation of human pancreatic cancer cell line Suit-II cells. The effect of annexin I on tumor growth was assessed by tumor growth curve and tumor weight records, and Westen blot and flow cytometry were used to examine the expression of annexin I after annexin I-knocking down.
The results of Western blot revealed that the expression of annexin I was significantly decreased in Suit-II cells transfected with pSilencer-annexin I-siRNA1, and almost completely inhibited in the cells transfected with pSilencer-annexin I-siRNA2 and pSilencer-annexin I-siRNA3. The growth of tumors transfected with annexin I-siRNA2 and annexin I-siRNA3 was inhibited by 76.6% and 68.4%, respectively, in comparison with that of tumor from the parent Suit-II cells. At 44 days after tumor cell inoculation, the tumor weight was 0.8987 g (transfected with annexin I-siRNA2) and 0.8992 g (transfected with annexin I-siRNA3), significantly lower (P < 0.001) than that of tumor from parent Suit-II cells (2.5866 g) and transfected with annexin I-siRNAN (2.4070 g).
annexin I promotes the growth and proliferation of pancreatic carcinoma cells in vivo and increases the ability of tumor formation in nude mice. The results of this study support that annexin I may become a potential target in gene therapy for this disease.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 01/2009; 30(12):897-900.
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Zhuan Zhou,
Yu-Liang Ran,
Hai Hu,
Jian Pan,
Zhi-Feng Li,
Li-Zhao Chen,
Li-Chao Sun,
Liang Peng,
Xi-Lu Zhao,
Long Yu, Li-Xin Sun,
Zhi-Hua Yang
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ABSTRACT: Esophageal cancer is characterized by rapid clinical progression and poor prognosis due to adjacent tissue invasion and distant organs metastasis at a very early stage. TM4SF3 (transmembrane 4 superfamily 3), a member of tetraspanin family, has been reported as a metastasis associated gene in many types of tumors. Herein, we described new properties of TM4SF3 in tumor metastasis, which suggested that this gene might be involved in esophageal carcinoma metastasis. Western blotting revealed that TM4SF3 was overexpressed in 57.1% (8/14) of esophageal carcinomas and esophageal carcinoma cell lines with high-invasive potential. Exogenous expression of TM4SF3 in two low-invasive esophageal carcinoma cell lines, KYSE150 and EC9706, significantly promoted cell migration and invasion. Upregulating TM4SF3 expression in EC9706 cells promoted xenograft tumor invading into surrounding tissues, enhanced lung metastasis, and shortened the lifespan of mice (median survival EC9706-TM4SF3 106.5 days versus EC9706-Vector 169.0 days, P < 0.0001) in a spontaneous metastasis model. Further studies demonstrated that ADAM12m was upregulated by TM4SF3 overexpression in vitro and in vivo. Abrogating up-expression of ADAM12m by siRNA significantly suppressed TM4SF3-mediated invasion. Together, these data from our studies indicated that overexpression of TM4SF3 in esophageal cancer conferred advantage to the invasion and metastasis of this destructive disease. Upregulated expression of ADAM12m by TM4SF3 might play a key role in TM4SF3-mediated invasion and metastasis. TM4SF3 and ADAM12m might be potential targets of esophageal carcinoma for anti-metastasis therapy.
Clinical and Experimental Metastasis 01/2008; 25(5):537-48. · 3.52 Impact Factor
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ABSTRACT: To investigate the protective effects of ginkgolides on glucose deprivation-induced apoptosis in PC12 cells and the mechanism underlying the protective effect.
PC12 cells were treated under glucose deprivation, and the proliferation was determined by tetrazolium (MTT) assay. Furthermore, the mRNA levels of Bcl-2, Bax, c-myc were measured by Fluorescence Quantitative PCR (FQ-PCR).
Ginkgolides could markedly inhibit the injury of glucose deprivation on the PC12 cells and increase the cell proliferation compared with the model groups (P <0.01). Ginkgolides could up-regulate Bcl-2 and down-regulate Bax and c-myc at 12 h, respectively. There were no significant differences in the Bcl-2 and Bax levels in both groups at 24 h, and ginkgolides only reduced the elevation of c-myc from 4. 32-fold to 2. 87-fold at this time.
Ginkgolides are able to protect the injured PC12 cells against cell apoptosis. During the early period of glucose deprivation, Bcl-2, Bax and c-myc were regulated to inhibit cell apoptosis by ginkgolides. After that, ginkgolides seems inhibit the apoptosis through attenuating the elevation of c-myc.
Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica 03/2007; 32(6):532-5.
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ABSTRACT: Total rhubarb anthraquinones (TRAs) are the active therapeutic components from the rhizomes of Rheum palmatum L. (Polygonaceae), which are widely used in traditional Chinese medicines (TCMs) and have been reported to have cell toxicity recently. This study focuses on the toxicity of TRAs on Sprague Dawley (S.D.) rats. TRAs administrated per os for 13 weeks induced nephrotoxicity on S.D. rats as renal tubule epithelial cells swelled and denatured in tissue slice examination. After high-density oligonucleotide microarrays scanning, we have identified mitogen-activated protein kinase (MAPK) kinase 6 to be the target gene which causes cell cycle arrest and proliferation inhibition and contributes to nephrotoxicity on S.D. rats.
Journal of Ethnopharmacology 10/2006; 107(2):308-11. · 3.01 Impact Factor
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ABSTRACT: Thrombin and factor Xa are key players in the process of arterial thrombi formation and lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) is a cell surface endocytosis receptor for atherogenic oxidized LDL (ox-LDL). Here we investigate whether thrombin and factor Xa can induce LOX-1 protein expressions in cell-associated forms and soluble forms in cultured bovine aortic smooth muscle cells (BSMCs).
BSMCs were treated with thrombin or factor Xa in the presence or absence of AG1478, an epidermal growth factor (EGF) receptor-associated tyrosine kinase inhibitor. Total cell lysates and concentrated culture medium were then analyzed by Western blot using a mouse anti-LOX-1 monoclonal antibody.
LOX-1 protein levels in cell lysates and culture medium were significantly increased by thrombin and factor Xa in a concentration- and time-dependent manner. Upregulation of LOX-1 protein expressions in cell lysates and concentrated culture medium was observed at concentrations above 2.0 and 3.0 U/ml of thrombin and 50 and 100 nmol/L of factor Xa, respectively. Increased LOX-1 protein expressions in cell lysates and cell culture medium were detectable as early as 4 h and peaked at 12 h after treatment with thrombin or factor Xa. LOX-1 expression induced by thrombin and factor Xa could be blocked by pretreatment with AG1478.
Thrombin and factor Xa can act as LOX-1 inducers via tyrosine kinase activation.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 04/2006; 34(3):262-6.
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ABSTRACT: CYP6F1 (GenBank/EMBL accession No. AY662654), a novel gene with a complete encoding sequence in the cytochrome P450 family 6, was cloned and sequenced from deltamethrin-resistant 4th instar larvae of Culex pipiens pallens. The cDNA sequence of CYP6F1 has an open reading frame of 1527 bp, which encodes a putative protein of 508 amino acid residues. The deduced amino acid sequence of CYP6F1 indicated that the encoded P450 has conserved domains of a putative membrane-anchoring signal, putative reductase-binding sites, a typical heme-binding site, an ETLR motif and substrate recognition sites. Semi-quantitative RT-PCR analysis indicated that the CYP6F1 gene was expressed to a greater extent in the deltamethrin-resistant strain than in the susceptible strain of Cx. pipiens pallens. The expression levels of the CYP6F1 gene in the deltamethrin-resistant 1st, 2nd, 3rd, 4th instar larvae and adult female mosquitoes differed, with highest expression levels in the 4th instar larvae. In addition, the CYP6F1 gene was stably expressed in mosquito C6/36 cells, and the expected 61.2 kDa band was identified by Western blotting. The cells transfected with CYP6F1 had an increased resistance to deltamethrin as compared with control cells. These results indicate that CYP6F1 is expressed at higher levels in the deltamethrin-resistant strain, and may confer some insecticide resistance in Cx. pipiens pallens.
Acta Biochimica et Biophysica Sinica 06/2005; 37(5):317-26. · 1.38 Impact Factor
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ABSTRACT: This study was designed to examine the level of serum vascular epithelial growth factor (VEGF) and VEGF expression in the patients with ovarian epithelial carcinoma (EOC) and to evaluate the relationship between VEGF and the clinicopathological factors.
Seventy-three patients with ovarian epithelial tumor were selected as study group, including 24 benign epithelial ovarian tumor (BET), 7 borderline epithelial ovarian tumor (BOT), 42 EOC. Twenty women without obvious gynecologic diseases were selected as serum control group (CON). VEGF expression in the epithelial ovarian tumor tissues from 73 patients were analyzed immunohistochemically. Serum VEGF in 71 patients and ascite VEGF in 10 patients were detected by enzyme-linked immunosorbent assay (ELISA) and 7 cases with EOC were continuously determined after operation.
(1) Positive immunostaining of VEGF was observed in 86.3% of EOC, which was significantly higher than that of BOT (66.67%, P < 0.005) and BET (37.5%, P < 0.005). (2) There were significant differences in serum VEGF level among BET, BOT, and EOC group (P < 0.01). Serum VEGF levels before operation in patients with EOC were significantly higher than those with BOT, BET, and CON (P < 0.01). Serum VEGF levels in EOC patients at advanced stage (stage III or IV), low differentiation (G3) were apparently higher than those at early stage (stage I or II) (P < 0.05) and high differentiation (G1, G2) (P < 0.01), respectively. Serum VEGF levels decreased after the successful removal of tumor in ovarian cancer patients. The serum VEGF levels were re-elevated during relapse in three patients.
(1) The elevated serum VEGF levels and increased VEGF expression in EOC were associated with its maligment behavior. (2) Serum VEGF could be used as a marker for monitoring the clinical course of the patients with epithelial ovarian carcinoma.
Ai zheng = Aizheng = Chinese journal of cancer 01/2003; 22(1):58-61.
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ABSTRACT: To demonstrate effects of antisense VEGF(165) to suppress esophageal cancer cells and to improve efficacy of the gene therapy of tumor by using hypoxic environment, hypoxia response element (HRE) was cloned from promoter of VEGF by PCR and employed to construct an eukaryotic expression vector containing luciferase and antisense VEGF(165) by using recombinant DNA techniques. The recombinant vectors were transfered into esophageal cancer cells by lipofectin methods, and hypoxia inducible reporter gene expression was determined by luminometer and the expression of antisense VEGF was evaluated indirectly by ELISA that detected of VEGF. The esophageal cells tansfected by antisense VEGF(165) gene were transplanted into nude mice, in order to evaluate the suppressive effect of antisense VEGF(165). Our results showed that, in vitro, hypoxia increased expression of reporter gene to 3 780 % and enhanced greatly expression of antisense VEGF. In vivo, the growth of esophageal cancer cells transfected by antisense VEGF in the vector containing HRE was suppressed more significantly, with suppression rate being 71.1%, than that by the vector without HRE, whose inhibiting rate 56.1%. It was concluded that antisense VEGF(165) suppressed significantly growth of esophageal cancer, and by using a gene expression vector containing HRE, the expression of target genes could be regulated autonomously by hypoxic environment of tumor and the efficiency of gene therapy could be greatly improved.
Sheng wu hua xue yu sheng wu wu li xue bao Acta biochimica et biophysica Sinica 10/2002; 34(5):625-9.
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ABSTRACT: NY-ESO-1 is a tumor antigen from cDNA library of esophageal carcinoma. However, there was no report about its expression in the tissue of esophageal carcinoma. In the current study, the authors examined the frequency of the NY-ESO-1 gene expression in esophageal carcinoma in order to determine whether NY-ESO-1 antigen-based vaccine therapy be available for the patients with esophageal carcinoma.
Reverse transcriptase and polymerase chain reaction amplification techniques were utilized to assay 30 esophageal carcinoma tissues and the matched adjacent normal esophageal tissues for expression of NY-ESO-1 gene. And the cDNA sequence of NY-ESO-1 was cloned from esophageal carcinoma tissues by molecular cloning techniques.
Out of 30 esophageal carcinoma tissues, 50% expressed NY-ESO-1 gene while no expressed in the matched adjacent normal esophageal tissues. The sequence of NY-ESO-1 cloned was identical to the sequence of that from GenBank.
NY-ESO-1 gene is expressed highly in esophageal carcinoma and NY-ESO-1 antigen can be recognized by cytolytic T lymphocytes when presented by HLA-class-I molecular.
Ai zheng = Aizheng = Chinese journal of cancer 06/2002; 21(5):469-72.
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ABSTRACT: Human inhibiting angiogenesis factor-1(HIAF-1) expressed in E coli. shown the activity of inhibiting the angiogenesis of tumors. This study was designed to investigate the expression of HIAF-1 in insect cells and to elucidate its biological activity.
Recombinant baculovirus expression vector pAcuW51-HIAF-1 was constructed by recombinant DNA technique and cotransfected with linearized baculovirus DNA into sf9 cells to produce recombinant virus. The expression of recombinant HIAF-1 in insect cells infected by recombinant virus was detected by SDS-PAGE and Western blot. The recombinant protein was purified by affinity chromatography. In vitro endothelial proliferation inhibiting activity of recombinant HIAF-1 was examined by MTT method, its antitumor activity in vivo was studied in human esophageal cancer transplanted in nude mice.
HIAF-1 was effectively expressed in insect cells as 26 KD fusing protein and its expression level was about 5-10% of insect cellular total soluble proteins. Recombinant HIAF-1 protein could inhibit endothelial cell proliferation in vitro with IC50 value of 3.1 micrograms/ml and inhibited remarkably growth of human esophageal cancer transplanted in nude mice.
The recombinant HIAF-1 with better activity was successfully expressed in insect cells and establish a base for clinical application.
Ai zheng = Aizheng = Chinese journal of cancer 04/2002; 21(3):245-8.
