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Biomedical subjects

Ding Ma

Publications and source records attributed to Ding Ma.

At least 55 records · Page 3Linked to original sources
PubMed2005

The synergic effect between Mo species and acid sites in Mo/HMCM-22 catalysts for methane aromatization.

The acid properties of Mo/HMCM-22 catalyst, which is the precursor form of the working catalyst for methane aromatization reaction, and the synergic effect between Mo species and acid sites were studied and characterized by various characterization techniques. It is concluded that Brønsted and Lewis acidities of HMCM-22 are modified due to the introduction of molybdenum. We suggest a monomer of Mo species is formed by the exchange of Mo species with the Brønsted acid sites. On the other hand, coordinate unsaturated sites (CUS) are suggested to be responsible for the formation of newly detected Lewis acid sites. Computer modelling is established and coupling with experimental results, it is then speculated that the effective activation of methane is properly accomplished on Mo species accommodated in the 12 MR supercages of MCM-22 zeolite whereas the Brønsted acid sites in the same channel system play a key role for the formation of benzene. A much more pronounced volcano-typed reactivity curve of the Mo/HMCM-22 catalysts, as compared with that of the Mo/HZSM-5, with respect to Mo loading is found and this can be well understood due to the unique channel structure of MCM-22 zeolite and synergic effect between Mo species and acid sites.

Acids↗
PubMed2005

Effect of the cyclin-dependent kinases inhibitor p27 on resistance of ovarian cancer multicellular spheroids to anticancer chemotherapy.

PURPOSE: A low proliferating fraction in solid tumors limits the effectiveness of cell-cycle-dependent chemotherapeutic agents. To understand the molecular basis of such resistance, we examined the expression of the cyclin-dependent kinases inhibitor p27, and relationship with drug resistance and P-gp expression in ovarian cancer multicellular spheroids. METHODS: We cultured ovarian cancer cells (A2780 and CAOV3) as multicellular spheroids and examined the expression of p27 and P-glycoprotein (P-gp) by western blot, flow cytometry and confocal. We also analyzed the cell-cycle distribution by flow cytometry. In addition, trypan blue exclusion testing and cell apoptosis analysis were used to detect the sensitivity to Taxol. RESULTS: When transferred from monolayer to three-dimensional culture, a consistent upregulation of p27 protein and P-gp protein was observed in ovarian cancer cell lines. Compared with monolayer cells, there was a significant increase of G0-G1 phase cells and decrease of S and G2-M phase cells in spheroid cells. Aggregates of cells showed higher cell viability than monolayer cells. Antisense oligodeoxynucleotide (ASON) -mediated downregulation of p27 reduced intercellular adhesion, increased cell proliferation, downregulated P-gp expression and sensitized cells to Taxol. CONCLUSIONS: Our results implicate that p27 serves as a regulator of drug resistance in ovarian tumors. ASON-mediated alteration of p27 reverses resistance of ovarian cancer to anticancer agents that are associated with increased sensitivity of ovarian cancer cells to chemotherapeutic agents.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Value and feasibility of HPV DNA test in cervical scraping smears.

To investigate the reliability and feasibility of human papillomavirus (HPV) DNA test in cervical scraping smears with polymerase chain reaction (PCR), 131 cases of cervical scraping specimens were collected, and the positive rates and accuracy of HPV infection were determined in normal subjects and cervical cancer patients. GP5+/GP6+ and E7 primer pairs designed for detecting HPV L1 and HPV type 16 E7 were tested in this study. Our results showed that positive rates of HPV DNA in normal population and cervical cancer patients were 32.99% and 73.53% respectively and there was significant difference between them (P < 0.001). In normal subjects, detection rates of HPV DNA with GP5+/GP6+ and E7 primer pairs were 27.84% and 16.49% respectively, with statistically significant difference between them (P > 0.05). However the detection rates in cervical cancer patients were 38.24% and 67.65% for the two markers, with a significant difference found between them (P < 0.05). It is concluded that HPV DNA test with PCR for cervical scraping smears was feasible. GP5+/GP6+ primer pairs may be a useful probe to screen HPV infection in normal population, but they are not sensitive enough in cervical cancer patients. It is suggested that high risk type HPV DNA test was very useful in population with high risk of cervical cancer.

Capsid Proteins↗
PubMed2005

Inhibitory effect of coxsackie adenovirus receptor on invasion and metastasis phenotype of ovarian cancer cell line SKOV3.

Full-length coxsackie adenovirus receptor (CAR) eukaryotic expression plasmid was transfected into an ovarian cell line, SKOV3, and its effect on the change of malignant metastasis phenotype was explored. CAR mRNA and protein expression levels among 4 ovarian cancer cell lines (A2780, SKOV3, SW626, CAOV3) and the positive control 293 (a transformed human embryo kidney cell line) was detected by using semi-quantitative RT-RCR and Western blot and compared. CAR-negative SKOV3 was transfected with the eukaryotic expression plasmid containing a full-length CAR cDNA and mock-vector respectively. The positive clones were screened by G418. The biological behavior changes of positive transfected cells were gauged by colony formation in soft agar assay and cell adhesion assay. Among the cell lines, there were obviously different CAR expression levels. CAR could not be detected in SKOV3. In transfected cell group, CAR expression was enhanced obviously as compared with non-transfected or mock-transfected groups. Cell adhesion in the transfected group was promoted. The number of colony formation was reduced significantly in transfected groups (25.32 +/- 8.91) as compared with that in non-transfected group (88.75 +/- 13. 98) and mock-transfected group (82.53 +/- 19.37). Among the 4 ovarian cancer cell lines, CAR expression level was variable. Exogenous CAR expression had a potential role in inhibiting the malignant metastasis phenotype of ovary cancer cells.

Cell Line, Tumor↗
PubMed2005

Construction of antisense MT1-MMP vector and its inhibitory effects on invasion of human ovarian cancer cells.

Membrane-type 1 matrix metalloproteinase (MT1-MMP/MMP-14) plays crucial roles in tumor cell growth, invasion, and angiogenesis. To clarify whether the endogenously expressed MT1-MMP in metastatic human ovarian carcinoma cell lines SKOV3 plays a critical role in tumor cell invasiveness, antisense MT1-MMP cloned in eukaryotic expression vector pMMP14as was transferred into SKOV3 cells. 48h after transfection, decreased expression of endogenous MT1-MMP protein was detected in pMMP14as-transfected SKOV3 cells and the activation of pro-MMP2 was inhibited markedly. The mean percentage of invasive cells was (62.50 +/- 5.30) % in pMMP14as-transfected cells, which was obviously less than that (97.20 +/- 6.90) % in the control. Thus, antisense MT1-MMP effectively inhibited the endogenous MT1-MMP expression and the invasiveness in SKOV3 cells, suggesting that MT1-MMP may be a therapeutic target molecule for human invasive ovarian cancers.

Cell Line, Tumor↗
PubMed2005

Regulation of HtrA2/Omi by X-linked inhibitor of apoptosis protein in chemoresistance in human ovarian cancer cells.

OBJECTIVE: Development of cisplatin resistance by cancer cells is a major hurdle in successful treatment of human ovarian cancer. However, the mechanism of cisplatin resistance in ovarian cancer cells remains unclear. In this study, we have examined the possible role of X-linked inhibitor of apoptosis protein (Xiap) in the development of cisplatin resistance in ovarian cancer cells and investigate if suppressed cytosolic high temperature required protein A (HtrA2/Omi) level is an important factor in cisplatin resistance in ovarian cancer. METHODS: Cisplatin-sensitive (A2780 and COC1) and -resistant (A2780/DDP and COC1/DDP) ovarian cancer cells were cultured for different durations (0-24 h) and with different cisplatin concentrations (0-20 muM). Xiap content and cytosolic HtrA2/Omi content were analyzed by Western blot. Antisense oligonucleotides were used to downregulate Xiap content in ovarian cancer cells. RESULTS: Cisplatin decreased Xiap content and increased cytosolic HtrA2/Omi content and caspase-3 activity in cisplatin-sensitive ovarian cancer cell lines (A2780 and COC1), but not in the resistant variants (A2780/DDP and COC1/DDP). Downregulation of Xiap by antisense Xiap oligonucleotides increased caspase-3 activity and sensitized cisplatin-resistant cells to cisplatin treatment. Cytosolic HtrA2/Omi level increased while Xiap was downregulated in cisplatin-resistant ovarian cancer cells. CONCLUSION: Development of cisplatin resistance may be due to Xiap neutralizing caspase-3 activation and lower cytosolic HtrA2/Omi level in response to cisplatin in human ovarian cancer cells. Cytosolic HtrA2/Omi level is partly regulated by Xiap in ovarian cancer cells.

Adenocarcinoma↗
PubMed2005

[Effects of chemokine receptor and its ligand on migration of ovarian cancer cells].

BACKGROUND & OBJECTIVE: Chemokine receptors express on many tumor cells, and closely correlate with migration and metastasis of tumor cells. This study was to investigate expressions of chemokine(C-X-C) receptor 4 (CXCR4) and chemokine (C-X-C motif) ligand 12 (CXCL12) in human ovarian epithelial tumor cells, and their effects on migration of tumor cells. METHODS: Expression of CXCR4 mRNA and protein in 15 specimens of epithelial ovarian cancer tissue, ovarian cancer cell line CAOV3, endothelial cell line HUVEC, and 10 specimens of normal ovary tissue were evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot. Expression of CXCL12 mRNA in retroperitoneal lymph nodes, and smooth muscle of fallopian tube from the same 15 epithelial ovarian cancer patients was tested by RT-PCR, quantity of CXCL12 in ascites of 15 patients was assayed using ELISA. Boyden Transwells was used to analyze effects of CXCL12, and cancerous ascites on chemotaxis of CAOV3, and HUVEC cells. RESULTS: (1) Expression levels of CXCR4 mRNA in ovary cancer tissues, CAOV3 cells, and HUVEC cells were 2.30+/-1.12, 1.89+/-1.20, and 1.68+/-1.11, respectively; those of CXCR4 protein were 1.35+/-0.14, 1.86+/-0.34, and 1.96+/-0.23, respectively; CXCR4 mRNA and protein can't be detected in normal ovarian tissues. (2) In 15 ovarian cancer patients, concentrations of CXCL12 in ascites were 632-9 326 pg/ml, and CXCL12 mRNA level in retroperitoneal lymph nodes was 1.14+/-0.87, CXCL12 mRNA can't be detected in smooth muscle of fallopian tube. (3) Recombinant human CXCL12 induced migration of CAOV3, and HUVEC cells, the chemotactic indices (CI) were 3.9+/-1.2, and 4.1+/-1.6, significantly higher than those of control (1.0+/-0.4, and 1.1+/-0.7) (P<0.05)u cancerous ascites induced migration of CAOV3 cells with CI of 1.9+/-0.8, significantly higher than that of control (P<0.05). CONCLUSION: CXCR4 and CXCL12 may play roles in metastasis of epithelial ovarian cancer by promoting migration of tumor cells and endothelial cells.

Adult↗
PubMed2005

[Changes in telomerase activity decreases in MCF-7 cells during apoptosis induced by sodium butyrate].

OBJECTIVE: To investigate telomerase activity of MCF-7 mammary cancer cells during apoptosis induced by sodium butyrate (SB) in vitro and its mechanism. METHODS: The proliferative activity of MCF-7 cells was assessed by morphology and MTT assay. Cell apoptosis was confirmed by DNA fragmentation and phosphatidylserine (PS) externalization. Telomerase activity was examined by TRAP-ELISA. The expression status of telomerase subunits was analyzed by RT-PCR. RESULTS: A time- and dose-dependent inhibition was detected in MCF-7 cells treated with SB. At 72 hr after SB (2.5 mmol/L) treatment, MCF-7 cells were apoptotic with a rate of 84.3% by flow cytometric assay (AnnexinV/PI double staining). Apoptosis was also confirmed by DNA fragmentation. Telomerase activity and expression level of hTERT, the key subunit of telomerase, decreased at 24-hour time point after SB treatment. No significant changes were observed in the expression of hTR and hTP, the other two subunits of telomerase. CONCLUSION: Telomerase activity decreases in MCF-7 cells during apoptosis induced by sodium butyrate. The underlying mechanism might be related to the down regulation of hTERT transcription.

Apoptosis↗
PubMed2005

[Impact of hypoxia on taxol-induced apoptosis in human ovarian cancer cell line A2780 and its mechanism].

BACKGROUND & OBJECTIVE: Hypoxia, a feature and important living microenvironment of solid tumors, might be related to drug-resistance of tumors. This study was to establish a hypoxic model of ovarian cancer cell line A2780, and to investigate impacts of hypoxia and hypoxia inducible factor-1alpha (HIF-1alpha) on Taxol-induced apoptosis in A2780 cells. METHODS: Cobalt chloride (CoCl(2)), a chemical hypoxia inducer, was added in A2780 cells to develop a hypoxic model. A2780 cells were divided into 4 groups: group A (control), group B (normoxia plus Taxol), group C (hypoxia plus Taxol), and group D (hypoxia, Decoy plus Taxol). Decoy method was used to block the function of HIF-1alpha. Protein and mRNA levels of HIF-1alpha were detected by Western blot and reverse transcription-polymerase chain reaction (RT-PCR). Cell apoptosis was detected by TdT-mediated dUTP nick end labeling (TUNEL), and flow cytometry (FCM). RESULTS: CoCl(2) evidently increased protein level of HIF-1alpha, but had no effect on mRNA level of HIF-1alpha. Decoy didn't affect its expression. TUNEL showed that apoptotic index (AI) was significantly higher in group B,and group D than in group C after treatment of Taxol [(41.1+/-25.6)%,and (35.2+/-21.7)% vs. (24.1+/-15.2)%, P < 0.05]. The apoptosis rates detected by FCM displayed the same tendency as TUNEL results did. CONCLUSIONS: Hypoxia could weaken the effect of Taxol on inducing apoptosis of A2780 cells. HIF-1alpha might confer to resistance of cell apoptosis induced by Taxol.

Antineoplastic Agents, Phytogenic↗
PubMed2005

Induction of apoptosis in human ovarian epithelial cancer cells by antisurvivin oligonucleotides.

Survivin, an anti-apoptosis gene that is abnormally overexpressed in a variety of human tumors, may play an important role in the carcinogenesis and drug resistance of cancer. This study was designed to explore the effects of liposome-survivin antisense oligonucleotide (Lip-ASODN) on the growth and apoptosis of human ovarian cancer cell lines, A2780 and SKOV3. To investigate the use of survivin as a therapeutic target on ovarian cancer, we carried out transfections with Lip-ASODN to induce apoptosis in ovarian cancer cell lines, A2780 and SKOV3. The expression of survivin mRNA and relative protein were evaluated separately by quantitative real-time RT-PCR and Western blot analysis. Cell proliferation inhibition was determined by methyl thiazolyl tetrazolium (MTT) assay, and the induced cell apoptosis was examined using flow cytometry (FCM) after Lip-ASODN transfection. Our results showed that the overexpression of survivin led to infinite carcino-proliferation, and survivin expression in the survivin-positive ovarian cancer cell line A2780 and SKOV3 cells was significantly and gradually reduced when transfected with Lip-ASODN at concentrations of 200, 400 and 600 nM by degrees. Lip-ASODN transfection induced greater apoptosis rates in the human ovarian cancer cell lines A2780 and SKOV3 (p<0.05). The growth inhibition and apoptotic rates of tumor cells change when treated with different concentrations of Lip-ASODN. The cell growth inhibition peak rate was reached when increasing Lip-ASODN concentration to 600 nM. Furthermore, time course evaluation showed that survivin protein expression was inhibited by Lip-ASODN within 12 h after transfection. We concluded that down-regulation of survivin by a targeted antisense oligonucleotide appears to be an effective gene therapy approach in the treatment of ovarian cancer.

Apoptosis↗
PubMed2005

[Expression of human telomerase reverse transcriptase in cervix cancer and its significance].

OBJECTIVE: To investigate the expression of human telomerase reverse transcriptase (hTERT) mRNA and protein in cervix cancer, cervical intraepithelial neoplasia (CIN) and normal cervix. METHODS: Expression of hTERT mRNA and the other two subunits of telomerase, human telomerase RNA component (hTR), human telomerase-associated protein (hTP1) was determined by RT-PCR in 3 cervix cancer cell lines, 2 diploid cell lines, 38 cases of cervix cancer, 16 cases of CIN and 20 cases of normal cervix. Telomerase activity was also examined by telomeric repeat amplification protocol enzyme-linked immunosorbent assay (TRAP-ELISA). Expression of hTERT protein was detected in all the cell lines and 101 cases of paraffinized cervix tissue sections. RESULTS: hTERT mRNA expression was detected in all of the three cervix cancer cell lines, 81.6% of cervix cancer, 37.5% of CIN, 5.0% of normal cervix, while in neither of the two diploid cell lines. The other two subunits of telomerase were prevalently expressed in all of the cell lines and most cervix tissues. There was a strong correlation between hTERT mRNA expression and telomerase activity. Immunostaining also revealed that hTERT protein was expressed in all three cervix cancer cell lines, 65.5% of cervix cancer, 28.0% of CIN and 4.8% of normal cervix. CONCLUSION: Up-regulation of hTERT may play an important role in the development of CIN and cervix cancer, hTERT could be used as an early diagnostic biomarker for cervix cancer.

Carrier Proteins↗
PubMed2005

[Inhibitory effect of coxsackie adenovirus receptor on invasive and metastatic phenotype of ovarian cancer cell line SKOV3].

BACKGROUND & OBJECTIVE: Coxsackie and adenovirus receptor (CAR) was originally identified as the cellular receptor of 2,5-type adenovirus. Recent researches found that CAR is a subordinate cell adhesion molecule and plays an important role in the malignant phenotype changes of tumor cells. This study was to explore inhibitory effect of CAR on invasive and metastatic phenotype of ovarian cancer cell line SKOV3. METHODS: The expression of CAR in ovarian cancer cell lines SKOV3, CAOV3, SW626, and A2780 was detected by quantitative reverse transcription-polymerase chain reaction (RT-RCR) and Western blot. SKOV3 cells were transfected with the eukaryotic expression plasmid containing full-length CAR cDNA. The positive clones were screened by G418, and identified by RT-PCR, Western blot and ADV/GFP infection assay. The biological behavior changes of positively transfected cells were assessed by colony formation assay and cell adhesion assay. RESULTS: The expression of CAR was down-regulated in the 4 ovarian cancer cell lines, among which SKOV3 cells had no CAR expression. The mRNA and protein levels of CAR were obviously higher in CAR-transfected SKOV3 cells than in untransfected cells and mock-transfected cells; the adhesion ability of CAR-transfected SKOV3 cells was obviously enhanced. The colony formation count was significantly lower in CAR-transfected SKOV3 cells than in untransfected cells and mock-transfected cells (25.3+/-8.9 vs. 88.8+/-14.0, 82.5+/-19.4, P<0.05). CONCLUSION: Transfected CAR gene may enhance the adhesion ability of ovarian cancer SKOV3 cells, therefore, inhibit the malignant metastatic phenotype of SKOV3 cells.

Adenoviridae↗
PubMed2005

[Enhancive effect of histone deacetylase inhibitor trichostatin a on transfection efficiency of adenovirus in ovarian carcinoma cell line A2780].

BACKGROUND & OBJECTIVE: The presence of Coxsackie and adenovirus receptor (CAR) on target cell surface is required for efficient adenovirus transfection; lack or down-regulated expression of CAR on cancer cells is the main cause of inefficiency of adenovirus-based gene therapy. This study was to evaluate enhancive effect of trichostatin A (TSA), a histone deacetylase (HDAC) inhibitor, on the transfection efficiency of adenovirus in ovarian carcinoma cell line A2780, and explore its possible application to adenovirus-based gene therapy. METHODS: mRNA and protein levels of CAR on A2780 cells were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot before and after treatment of TSA. Transfection efficiency of adenovirus was valued by flow cytometry (FCM). In vitro antitumor effect of adenovirus/thymidine kinase (ADV/TK) was detected by MTT assay. RESULTS: After treatment of TSA, mRNA and protein levels of CAR on A2780 cells were obviously increased. Transfection rates of adenovirus were (1.24+/-0.14)% in untreated group, (7.58+/-0.32)% in 5 nmol/L of TSA treated group, and (7.94+/-0.28)% in 100 nmol/L of TSA treated groups. In vitro antitumor effect of ADV/TK was 4-10 folds in TSA (5 or 100 nmol/L) treated groups compared with that in untreated group. CONCLUSION: TSA could enhance transfection efficiency of adenovirus in ovarian carcinoma cells, and may be useful in gene therapy for ovarian carcinoma.

Adenoviridae↗
PubMed2005

[Effects of selected phages with specific peptide ligands on the biological behaviors of ovarian cancer cells].

OBJECTIVE: To evaluate the effects of the selected phages with the specific peptide ligands upon the biological behaviors of the ovarian cancer cells. METHODS: Two ovarian cancer cell lines, A2780 and SKOV3, were used in the study. They were divided into three groups respectively: study group, blank control group and negative control group. The effects of the phages were evaluated by trypan blue staining, flow cytometry, colony formation test, methyl thiazolyl tetrazolium (MTT) assay and Boyden chamber invasion assay. RESULTS: The average viability of ovarian cancer cells of study groups was (72.1 +/- 6.2)%, higher than that of negative control group (84.8 +/- 4.6, P < 0.05); the apoptosis ratio of the A2780 and SKOV3 cells of study groups increased (20.39% and 43.99% vs 0); the average colony formation rate of the ovarian cancer cells was of study groups 4%, lower than the control group (15%, P < 0.05); the inhibition rates of cell proliferation of A2780 and SKOV3 cells of study groups were 11.07% and 9.58%, significantly higher than that of their respective negative control (2.05% and 1.09%); the invasion index of the ovarian cancer cells decreased compared with the control. CONCLUSION: The selected phages down-regulate the growth, proliferation and invasion ability of the ovarian cancer cells to certain extent, the identified peptide ligands may play a role in tumorigenesis and metastatic transformation of ovarian cancers.

Apoptosis↗
PubMed2005

[Effect of transcriptional factor snail on epithelial-mesenchymal transition and tumor metastasis].

BACKGROUND & OBJECTIVE: Transcription factor Snail mediates epithelial-mesenchymal transition (EMT), and is associated with tumor metastasis. This study was designed to observe the enhancive effect of Snail and the reverse effect of antisense-Snail on EMT of tumor cells, and explore the role of Snail in tumor metastasis. METHODS: Snail cDNA was transfected into canine renal epithelial cell line MDCK; antisense-Snail was transfected into human breast cancer cell line MDA-MB231. The expression of epithelial markers E-cadherin, beta-catenin and Cytokeratin 18, mesenchymal marker Fibronectin, metastasis-related marker matrix metalloproteinase-2 (MMP-2), and RhoA were detected by Western blot. The metastatic potential of tumor cells was examined by in vitro cell wound model and Boyden chamber invasion assay. RESULTS: The invasion potential of MDCK cells was enhanced after transfection of Snail. The expression of E-cadherin, beta-catenin, and Cytokeratin 18 was significantly lower in Snail-transfected MDCK cells than in control cells (P < 0.05); the expression of Fibronectin, MMP-2, and RhoA was significantly higher in Snail-transfected cells than in control cells (P < 0.05). Inhibiting the expression of Snail with antisense-Snail in MDA-MB231 cells led to opposite results. CONCLUSION: Snail promotes EMT in normal epithelial cells, and inhibiting the expression of Snail may reverse EMT and suppress tumor metastasis.

Animals↗