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Xiao-qing Zhang

Publications and source records attributed to Xiao-qing Zhang.

8 recordsLinked to original sources
PubMed2006

[Study of growth inhibition of gastric cancer cells by sRNA targeting polo like kinase 1 in vitro and vivo].

OBJECTIVE: To observe the effect of polo like kinase 1 (plk1) gene depletion on the growth of gastric cancer cell line-MKN45 cells in vitro and vivo and discuss the feasibility and effectiveness of arranging plk1 as gene therapeutic target for gastric cancer. METHODS: The plk1 expression of MKN45 cells was inhibited by RNA interference (RNAi). The plk1 mRNA and protein level were measured by real-time quantitative PCR and western blotting, and the change of cell cycle distribution and apoptosis rate were detected by flow-cytometry, and the MKN45 cells proliferation was measured by MTT method. MKN45 cells treated with plk1 siRNA were transplanted subcutaneously in nude mice and their tumorgenesis ability were observed, the plk1 protein levels of the samples from nude mice in different groups were compared. RESULTS: After treatment with plk1 siRNA, plk1 mRNA and protein level decreased obviously in certain time, more MKN45 cells accumulated at G(2)/M (P < 0.05). Apoptosis rate of MKN45 cells treated with plk1 siRNA was higher than that of control cells at 48 h and 72 h (P < 0.05), and MKN45 cells proliferated slowly than control groups (P < 0.05), while the tumorgenesis ability obviously decreased, but the plk1 protein levels of the samples from nude mice in different groups were not different. CONCLUSIONS: siRNA targeting plk1 can inhibit the proliferation of MKN45 cells in vitro and vivo. Plk1 may be a novel therapeutic target for gastric cancer.

Animals↗
PubMed2006

[Inhibition of polo like kinase gene expression induces apoptosis in gastric cancer cells].

OBJECTIVE: To observe the effect of inhibition of polo like kinase1 (plk1) gene expression on apoptosis induction in gastric cancer cell line-MKN45 and discuss the vital role of plk1 proliferation and viability of gastric cancer cells. METHODS: The plk1 expression was inhibited by chemically synthesized siRNA. The plk1 mRNA and protein level were respectively measured by real-time quantitative PCR and Western blotting. The spindle morphological change was observed by immunofluorescence staining and confocal microscopy. The change of cell cycle distribution and apoptosis rate was detected by flow-cytometry. Pro caspase3 level was also detected by western blotting. RESULTS: After treatment by siRNA targeting plk1, plk1 mRNA and protein level decreased obviously, the cell mitotic spindle became obscure and lost cohesiveness, more MKN45 cells accumulated at G(2)/M phase (P< 0.05), apoptosis rate of plk1 siRNA treated MKN45 cells was higher than that of control cells at 48 h and 72 h (P< 0.05) with pro-caspase3 level decreasing at 72 h. CONCLUSIONS: Inhibition of plk1 gene expression induces apoptosis in MKN45 cells through the pathway of caspase3. Plk1 gene play a key role in viability of MKN45 cells.

Apoptosis↗
PubMed2006

[Mitotic arrest of gastric cancer cells induced by silencing of STK15 gene].

OBJECTIVE: To investigate the role of STK15 in regulating mitosis of gastric cancer cells (MKN45) by gene silencing through RNA interference mechanism. METHODS: RNA interference technique was used to inhibit STK15 expression in MKN45 cells. The expression levels of STK15 mRNA and protein were measured by real-time quantitative RT-PCR and Western blot respectively and cell morphological changes were investigated by reverse microscopy. In addition, cell cycle distribution and cellular proliferation were determined by flow-cytometry and MTT assay respectively. Finally, the mitotic phenotype of MKN45 cells was studied by immunofluorescence staining and confocal microscopy. RESULTS: Silencing of STK15 gene by RNA interference was confirmed by marked decrease of STK15 mRNA and protein levels in the treated MKN45 cells. This silencing correlated with rounding of the cells, decreasing of DNA content in G(2) phase (P < 0.05) and a lowered proliferation index (P < 0.05), along with alterations of mitotic phenotype of MKN45 (P < 0.05). CONCLUSION: STK15 gene may play a key role in regulating cellular mitosis and its inhibition by RNA interference leading to mitosis arrest in MKN45 cells.

Adenocarcinoma↗
PubMed2006

[Gene expression profiling of diffuse-type gastric cancer by cDNA microarray].

OBJECTIVE: To identify cancer-related genes in diffuse-type gastric cancer and to explore its molecular mechanism by cDNA microarray analysis. METHODS: A total of 22 pairs of diffuse-type gastric cancer tissue and the corresponding normal mucosa were taken and freshly frozen. cDNA microarray with 14,592 genes/ESTs was used. Genes were considered to be up- or down-regulated when the fluorescent intensity ratio between tumor and normal mucosa was over 2-fold in over 50% of the samples (P < 0.05). Hierarchical clustering of regulated genes was performed as a measure to study expressional similarity. Validation of array results was carried out by real time quantitative PCR (QPCR). RESULTS: Compared with those of corresponding normal mucosa, there were a total of 153 genes/ESTs up-regulated and 204 down-regulated in diffuse-type gastric cancer. Hierarchical clustering demonstrated that the genes belonging to the same subgroup displayed similar function. Most of the overexpressed genes were those related to cell adhesion, cell motility, matrix reconstruction, cell proliferation and/or signal transduction; while genes related to defense response, toxicoid metabolism, DNA repairing, nuclear-cytoplasmic transport and/or anti-apoptosis made up the main list of the underexpressed genes. Seven genes showed higher expression in TNM (T I + T II) group than in (T III + T IV) group. QPCR confirmed the array analysis results. CONCLUSION: Gene expression profiling by cDNA microarray analysis provides not only molecular understanding of biological properties of cancer, but may also be helpful in discovering new diagnostic markers and therapeutic targets in gastric adenocarcinoma.

Adenocarcinoma↗
PubMed2006

[Mitosis arrest caused by inhibition of PLK1 expression in gastric cancer MKN45 cells].

OBJECTIVE: To observe the effect of polo-like kinase 1 (PLK1) gene depletion on mitosis phenotype and elucidate its vital role in gastric cancer cell line (MKN45) mitosis. METHODS: The PLK1 expression in MKN45 cells was blocked by RNA interference (RNAi), the expression level of PLK1 mRNA and protein were measured by real-time quantitative PCR and Western blot, respectively. The morphological change of microtubules and mitosis phenotype in MKN45 cells were observed by immunofluorescence staining and laser confocal microscopy, the morphological changes of cells were observed by reverse microscopy, the variation of cell cycle distribution was detected by flow-cytometry. RESULTS: After RNAi targeting PLK1, PLK1 mRNA and protein level decreased obviously, the cell microtubules became obscure and lost cohesiveness, the mitosis phenotype also varied substantially (P < 0.05), more gastric cancer cells became rounded and showed G(2) phase cell DNA content (P < 0.05). CONCLUSION: PLK1 gene plays a key role in mitosis and its inhibition can lead to mitosis arrest in MKN45 cells.

Adenocarcinoma↗
PubMed2006

[Inhibition of serine/threonine kinase 15 gene expression induces apoptosis of gastric cancer cells].

OBJECTIVE: To observe the effect of inhibition of serine/threonine kinase15 (STK15) gene expression on apoptosis induction in gastric cancer cell line-MKN45 and discuss the role of STK15 in viability of gastric cancer cells. METHODS: The STK15 expression was inhibited by chemically synthesized siRNA. The STK15 mRNA and protein level were respectively measured by real-time quantitative PCR and western blotting,the change of cell cycle distribution and apoptosis rate were detected by flow-cytometry, cell morphological change was observed by Hoechst staining,and pro-caspase 3 level was also detected by western blot. RESULTS: After treatment by siRNA targeting STK15 after 48 h, STK15 mRNA and protein level decreased obviously. More MKN45 cells accumulated at G(2)/M phase (P< 0.05). The apoptosis rate of STK15 siRNA treated MKN45 cells was higher than that of control cells(P< 0.05) with the pro-caspase 3 level decreased. CONCLUSIONS: Inhibition of STK15 gene expression may induce apoptosis in MKN45 cells through the pathway of caspase3. STK15 gene play a key role in proliferation and viability of MKN45 cells.

Apoptosis↗
PubMed2002

[Relationship between expression of p27 and DNA ploidy in colorectal carcinoma].

BACKGROUND & OBJECTIVE: Cell cycle regulation changes in most of tumors. We can regard tumors as a kind of cell cycle diseases. p27 protein is a main negative cell cycle regulator, meantime it is an important prognosis factor of tumors. The significance of reduced expression and altered sbucelluar localization of p27 protein is unclear in progression of colorectal carcinoma. The relevance of p27 protein and DNA ploidy hasn't been reported in colorectal carcinoma. The study was designed to investigate the relationship between the expression of p27 protein and clinicopathological features, DNA ploidy in colorectal carcinoma. METHOD: The expression of p27 was observed in 40 colorectal cancer cases using immunohistochemical technique, and DNA content of cancer cells was analyzed using DNA imaging analysis system. RESULTS: The high p27 expression rate was 62.5% (25/40), while low expression rate was 37.5% (15/40). Low p27 expression was significantly associated with low tumor grade. (P < 0.05). In addition to nuclear staining, 32.5% (13/40) of the carcinoma displayed p27-positive immunoreactivity in cytoplasm. Cytoplasmic localization of p27 was association with late Dukes stage(P < 0.01) and high incidence of lymph node metastases(P < 0.05). The detective rate of polyploidy cell in the patients with p27 lower expression (22.2 +/- 11.3%) was significantly higher than that with p27 higher expression (8.0 +/- 7.7%, P < 0.001). CONCLUSION: Reduced expression and altered subcellular localization of p27 play a role in progression of colorectal carcinoma; one suppression tumor mechanism of p27 might be to prevent the acquisition of polyploid DNA content in colorectal carcinoma cells.

Adult↗