Biomedical subjects

Ding Ma

Publications and source records attributed to Ding Ma.

95 records · Page 6Linked to original sources

PubMed2002

[Monitoring impact of measurement of urinary beta-human chorionic gonadotropin on orthotopic implantation model of human ovarian carcinoma in athymic nude mice].

BACKGROUND & OBJECTIVES: Tumor orthotopic transplantation model has become the main carrier for tumor animal experiment. However, there was no convenient and reliable method to monitor tumor growth in animal body. This study was designed to evaluate the monitoring impact of urinary beta-human chorionic gonadotropin (beta-HCG) on tumor growth in orthotopic implantation model. METHODS: Pclone-beta-HCG stably transfected human ovarian carcinoma cell line A2780-CG was made as the orthotopic implantation model. The urinary beta-HCG/creatine ratio was continuously determined and plotted into curve, so as to indirectly know the rule of tumor growth in nude mice and the monitoring value of the ratio for intraperitoneal chemotherapy by cisplatin. RESULTS: The tumorigenesis time in beta-HCG system transfected tumor cell A2780-CG was similar to that in the original cell line. The content of urinary beta-HCG/creatine had a positive correlation to tumor weight in animal body (r = 0.98); After chemotherapy with cisplatin, the beta-HCG/creatine ratio showed progressively decreased. CONCLUSION: beta-HCG system could be used to sensitively and non-invasively monitor the tumor growth in orthotopic implantation model of human ovarian carcinoma in nude mice. Meanwhile, it provides a new convenient monitoring method for tumor treatment in the model.

Animals↗

PubMed2002

[Molecular mechanism of inhibition of sodium butyrate on activation of tumor associated aromatase promoters].

BACKGROUND & OBJECTIVE: Sodium butyrate, a histone deacetylase inhibitor, can inhibit tumor conditioned medium-induced levels of promoter II and I. 3-specific transcripts. This study was designed to investigate the action of sodium butyrate on promoter II and I. 3 activity, which can be directed to elucidation of local estrogen production in breast cancer. METHODS: Primary human adipose fibroblasts (HAF) treated with MCF-7 breast cancer cell-conditioned medium were used as a cell model system. Promoter II and I. 3 deletion luciferase constructs was transfected into HAF. Western blotting and electrophoretic mobility shift assay were performed to evaluate the effect of sodium butyrate on promoter II and I .3. RESULTS: Breast cancer cell-conditioned medium enhanced phosphorylation of activator transcription factor-2 (ATF-2) which was the main modulatory subtype in CREB/ATF-2 family. The effect of sodium butyrate on aromatase expression in breast tumor fibroblasts was mediated by inhibition of phosphorylation of ATF-2, and hence, the inhibition of binding of a transcriptional complex containing phosphorylated ATF-2, C/EBP beta and CREB binding protein (CBP) to promoter II/I. 3 regulatory region. CONCLUSIONS: Sodium butyrate reduces the level of aromatase mRNA arising from cancer-induced promoter region. The aberrant activation of promoter II and I. 3 in HAF is dependent on the phosphorylation of ATF-2.

Activating Transcription Factor 1↗

PubMed2002

[Relationship between expression of apoptosis-associated proteins and caspase-3 activity in cisplatin-resistant human ovarian cancer cell line].

BACKGROUND & OBJECTIVE: Cisplatin-based chemotherapy is an important way for treatment of ovarian cancer, but resistance to cisplatin is one of the reasons of treatment failure of ovarian cancer. This study was designed to investigate the relationship between apoptosis-associated proteins and caspase-3 activity as well as their effects on chemoresistance in human ovarian cancer cell lines. METHODS: The expression of apoptosis-associated proteins (bcl-2, bcl-xL, bax, bcl-xs), the activity of caspase-3 and cleavage of poly ADP-ribose polymerase (PARP) were determined with Western blot analysis in the cisplatin-resistant cell (COC1/DDP) and cisplatin-sensitive human ovarian cancer cell (COC1). The apoptotic ratios of COC1 and COC1/DDP were measured with flow cytometry after treated with different concentration of cisplatin. RESULTS: The expression of bcl-2 and bcl-XL in COC1/DDP cell was significantly higher than that in COC1 cell, whereas the expression of bax showed no change in COC1/DDP and COC1. There was no bcl-xs expression in both COC1 and COC1/DDP cells. The activity of caspase-3, the amount of PARP fragments, and apoptotic ratio in COC1/DDP reduced much more than COC1 did after treated with cisplatin. CONCLUSIONS: Cisplatin-resistance in human ovarian cancer cell lines may associated with the overexpression of anti-apoptotic protein bcl-2 and downregulation of caspase-3 activity, but not associated with the expression of bax and bcl-xs.

Antineoplastic Agents↗

PubMed2002

[Relationship between cytochrome c-mediated caspase-3 activity and chemoresistance in cisplatin-resistant human ovarian cancer cell lines].

OBJECTIVE: To investigate the effects of anti-apoptosis gene (bcl-X(L)), cytochrome c and caspase-3 activity on chemoresistance in cisplatin-resistant human ovarian cancer cell lines (A2780/DDP, COC1/DDP). METHODS: The expression of bcl-X(L) cisplatin treated cytochrome c and caspase-3 activity were monitored by RT-PCR and Western blot in cisplatin-resistant (A2780/DDP, COC1/DDP) and cisplatin-sensitive (A2780, COC1) cell lines. The apoptotic rates of A2780, COC1, A2780/DDP and COC1/DDP were detected with flow cytometry after having been treated by cisplatin. RESULTS: The expression of bcl-X(L) in A2780/DDP and COC1/DDP was significantly higher than that in A2780 and COC1 cells, whereas the expression of cytochrome c, caspase-3 activity and apoptotic rates of A2780/DDP and COC1/DDP were significantly reduced more than those of A2780 and COC1 after having been treated by cisplatin (P < 0.05). CONCLUSION: The overexpression of anti-apoptotic gene bcl-X(L), which downregulates cytochrome c and decreases caspase-3 activity, may be related to cisplatin-resistance in human ovarian cancer cell lines.

Antineoplastic Agents↗

PubMedDate not supplied

Inhibition of motile and invasive properties of ovarian cancer cells by ASODN against Rho-associated protein kinase.

p160ROCK, a kinase effector of Rho GTPase mediating RhoA-induced assembly of focal adhesions and stress fibers, plays an important role in the invasive process of various tumor cells. The purpose of this study was to investigate the role of p160ROCK in the invasive behaviors of human ovarian cancer cells and their metastasis. Transfection with a dominant-active form of p160ROCK mutant (p160ROCKDelta 3) enhanced cell migration and invasion of ovarian cancer cells, while antisense oligodeoxynucleotide (ASODN) against p160ROCK inhibited the motile and invasive properties of the cells. Our data suggested that p160ROCK was involved in ovarian cancer cell invasion and metastasis by facilitating cancer cell migration, and that p160ROCK might be a potential new effective target for preventing metastasis of ovarian cancer.

Actins↗