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ABSTRACT: We have recently reported that RhoA may regulate the invasion and metastasis of breast cancer cells as an upstream signal of ezrin in vitro. In this study, we examined the relationship of RhoA signaling activity with ezrin expression in breast cancer and its prognostic significance in patients with breast cancer.
Paraffin tumor sections of breast cancer were collected retrospectively from 487 patients diagnosed between 2001 and 2004. Immunohistochemical methods were used to detect the expression of RhoA, phosphorylated (activated) RhoA, and ezrin.
Ezrin overexpression was detectable in 15.2% of 487 invasive breast cancers. The majority (85.1%) of ezrin-overexpressing tumors coexpressed phosphorylated RhoA; 78.8% of tumors with phosphorylated RhoA cooverexpressed ezrin. Patients whose cancers showed overexpression of ezrin or expression of phosphorylated RhoA had shorter survival rates.
RhoA activation is important in human breast cancer due to its upregulation of ezrin; thus, agents that target phosphorylated RhoA may be useful in the treatment of tumors with ezrin overexpression.
Chinese medical journal 01/2013; 126(2):242-7. · 0.86 Impact Factor
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ABSTRACT: p33(ING1b), a newly discovered candidate tumor suppressor gene and a nuclear protein, belongs to the inhibitor of growth gene family. Previous studies have shown that p33(ING1b) is involved in the restriction of cell growth and proliferation, apoptosis, tumor anchorage-independent growth, cellular senescence, maintenance of genomic stability and modulation of cell cycle checkpoints. Loss of nuclear p33(ING1b) has been observed in melanoma, seminoma, papillary thyroid carcinoma, oral squamous cell carcinoma, breast ductal cancer and acute lymphoblastic leukemia. Inactivation and/or decreased expression of p33(ING1b) have been reported in various types of cancer, including head and neck squamous cell, breast, lung, stomach, blood and brain malignancies. Since little is known about the clinicopathological significance of p33(ING1b) in esophageal squamous cell carcinoma (ESCC), this study aimed to investigate the association of p33(ING1b) expression with clinicopathological variables and particularly interesting new cysteine-histidine rich protein (PINCH) in patients with ESCC. p33(ING1b) expression was examined by immunohistochemistry in 20 normal esophageal mucosa and in 64 ESCC specimens. The results revealed that the positive expression of p33(ING1b) protein in normal squamous cells was localized in the nucleus alone and the positive rate was 95%, while in ESCCs, the positive expression was mainly in the cytoplasm, together with nuclear expression, and the positive rate was 36% (P<0.0001). Furthermore, the cases with lymph node metastasis showed a higher frequency of positive cytoplasmic expression than those without metastasis (P=0.001). The cytoplasmic expression of p33(ING1b) was positively related to PINCH expression (P<0.0001) in ESCC, and the cases positive for both proteins had a high lymph node metastasis rate (P=0.001). In conclusion, p33(ING1b) cellular compartmental shift from the nucleus to the cytoplasm may cause loss of normal cellular function and play a central role in the tumorigenesis and metastasis of ESCC.
Oncology letters 01/2013; 5(1):161-166. · 0.11 Impact Factor
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ABSTRACT: The mammalian target of rapamycin/eukaryotic translation inititiation factor 4E binding protein 1 (mTOR/4E-BP1) transduction pathway is activated in a range of malignant cancers, but its role in human gastric cardiac adenocarcinoma (GCA) has not been well defined. The present study used western blotting and reverse transcription polymerase chain reaction (RT-PCR) to assess the expression of mTOR, 4E-BP1 and eukaryotic translation initiation factor 4E (eIF4E) at the protein and mRNA levels in 33 cases of GCA and paired adjacent normal gastric mucosal tissues. The expression of mTOR at the protein level in GCA was significantly lower than that in the corresponding normal gastric mucosa (0.296±0.27 vs. 1.348±0.80, P<0.05), but the ratio of p-mTOR to mTOR was significantly increased in tumor tissues (1.425±1.07 vs. 0.450±0.24, P<0.05). The expression of 4E-BP1 was significantly decreased in GCA compared with normal tissues (p<0.05), while the levels of phosphorylated 4E-BP1 (p-4E-BP1) were markedly increased in tumor tissues (p<0.05). The levels of phosphorylated eIF4E (p‑eIF4E) were significantly higher in the tumors in comparison to the corresponding normal tissues (1.822±0.63 vs. 0.997±0.38, P<0.05), and the levels of p-eIF4E were closely correlated with lymph node metastasis (p<0.05). The mTOR/4E-BP1 signaling pathway is activated in GCA, with mTOR activated mainly through increased mTOR phosphorylation rather than protein overexpression.
Molecular Medicine Reports 11/2012; · 0.42 Impact Factor
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ABSTRACT: Objective: Particularly interesting new cysteine-histidine rich protein (PINCH) is an important component of the local adhesion complexes and upregulated in several types of malignancies, and involved in the incidence and development of tumours. PINCH expression is also independently correlated with poorer survival in patients with colorectal cancer. However, there is no study of PINCH in gastric cancer, therefore, the aim of this project was to investigate PINCH expression and its clinicopathological significance in gastric adenocarcinoma. Patients and methods: PINCH expression was immunohistochemically examined in normal gastric mucous (n=30) and gastric adenocarcinoma (n=73), from gastric cancer patients. Results: PINCH expression in the associated-stroma of gastric cancers was heterogeneous, and its positive rate (75%) was higher than that of normal gastric mucosa (43%, x^{2} =9.711, p=0.002). The stronger staining was observed at the invasive edge of tumour when compared to the inner area of tumour. The rate of positive PINCH (88%) in the cases with lymph node metastasis was higher than that (52%) in the cases without metastasis ( x^{2} =11.151, p=0.001). PINCH expression was not correlated with patients' gender, age, tumour size, differentiation and invasion depth (p> 0.05). Comclusion: PINCH protein might play an important role in the tumourigenesis and metastasis of gastric adenocarcinoma.
Disease markers 09/2012; · 1.64 Impact Factor
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ABSTRACT: To evaluate the H. pylori and Epstein-Barr virus infection in cardiac and distal gastric adenocarcinoma tissues in residents in Cixian county, a high risk area of esophageal cancer in Hebei province, and to explore the putative role of H. pylori and Epstein-Barr virus infection in the carcinogenesis of adenocarcinoma at different subsites of stomach.
H. pylori and Epstein-Barr virus latent membrane protein 1 (EBV-LMP1) immunopositivities were determined by Elivision(TM) plus immunohistochemical staining in 190 gastric adenocarcinoma tissues including 144 cases of cardiac adenocarcinoma and 46 cases of distal gastric adenocarcinoma. The relationship between H. pylori and Epstein-Barr virus infection and the subsite, Laurén type as well as other clinicopathological features of gastric adenocarcinoma were analyzed.
No significant difference was found between the H. pylori detection rates in cardiac and distal gastric adenocarcinomas(56.9% vs. 65.2%, P > 0.05). The detection rate of H. pylori in intestinal type was significantly higher than that in the diffuse type distal gastric adenocarcinomas (71.8% vs. 28.6%, P < 0.05). No positive expression of EBV-LMP1 was found in the gastric adenocarcinomas in this study.
No significant differences in H. pylori and EBV-LMP1 infections were found between cardiac and distal gastric adenocarcinomas in Cixian county. H. pylori infection is related with the intestinal type of distal gastric adenocarcinoma.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 06/2012; 34(6):446-9.
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ABSTRACT: Sterigmatocystin (ST) is a toxic metabolite mainly produced by the fungi Aspergillus nidulans and Aspergillus versicolor. ST is considered a potent carcinogen, mutagen and teratogen. However, over the past few years, it has been demonstrated that it is less acutely toxic to rodents in vivo. In this study, we evaluated the putative effects of ST on the expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-12 at mRNA levels in murine peripheral blood mononuclear cells (mPBMCs) and peritoneal macrophage cells and on the serum TNF-α and IL-6 levels in BALB/c mice. Our results show the downregulation of TNF-α, IL-6 and IL-12 mRNA expression in mPBMCs and peritoneal macrophage cells using semi-quantitative reverse transcription-polymerase chain reaction following ST treatment by intraperitoneal injection. Additionally, serum TNF-α and IL-6 levels were also decreased as shown by enzyme-linked immunosorbent assay (ELISA). These results suggest that ST contamination has negative immunomodulatory effects through the downregulation of cytokine expression and secretion.
Molecular Medicine Reports 02/2012; 5(5):1318-22. · 0.42 Impact Factor
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ABSTRACT: Sterigmatocystin (ST), a mycotoxin commonly found in foodstuff and feedstuff, has been shown to be a carcinogenic mycotoxin in animal models. Many studies showed that the high level of ST contamination in grains might be related to the high incidence of gastric carcinoma in rural areas of China. However, up to now, the potential effects of ST on human gastric epithelium cells remain largely unknown. In this study, we explored the effects of ST on cell-cycle distribution and the regulatory mechanism in immortalized human gastric epithelium cells (GES-1).
The effects of ST on the cell cycle distribution of GES-1 cells were determined with flow cytometric (FCM) analysis, Giemsa staining and immunofluorescence staining, while that on the expression of related gene-Cdc25C, Cdc2, CyclinB1 and the complex of CyclinB1-Cdc2 were studied with Western blot, reverse transcription polymerase chain reaction (RT-PCR) and immunoprecipitation assay respectively. We found that ST induced GES-1 cells arrested at G2 phase by regulating the expression of Cdc25C, Cdc2, CyclinB1 and the formation of CyclinB1-Cdc2 complex. Further study suggested JNK, ERK and PI3K/AKT/mTOR pathways to be involved in the process of G2 arrest induced by ST. The specific inhibitors of JNK and ERK reversed the role of ST, whereas that of PI3K/AKT/mTOR reinforced the effect of ST on cell-cycle distribution.
This study demonstrates that JNK, ERK and PI3K/AKT/mTOR pathways participated in the G2 arrest induced by ST through the deregulation of CyclinB1, Cdc2 and Cdc25C. It may play some roles in the gastric carcinogenesis in ST exposure populations.
Molecular Nutrition & Food Research 02/2011; 55(5):749-60. · 4.30 Impact Factor
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ABSTRACT: To study the possible role of JNK1, Raf-1 and Livin in the carcinogenesis of sporadic colorectal tubular adenoma.
Immunohistochemical staining was used to detect the expression of JNK1, Raf-1 and Livin proteins in 65 sporadic colorectal tubular adenomas with dysplasia of varying degrees and 22 colorectal tubular adenoma with cancerous area.
In normal colorectal mucosa, colorectal tubular adenoma with dysplasia and colorectal tubular adenoma with cancerous area, the positive rate of JNK1, Raf-1 and Livin expression was increased gradually. The positive expression of JNK1, Raf-1 and Livin was all significantly higher in the cases of colorectal tubular adenoma with dysplasia or with cancerous area than that in normal colorectal mucosa (P < 0.05), and the positive expression of JNK1, Raf-1 and Livin was significantly higher in colorectal tubular adenoma with cancerous area than that in colorectal tubular adenoma with dysplasia of different degrees (P < 0.05). In the cases of colorectal tubular adenoma with dysplasia of varying degrees, the positive expression of Raf-1 was increased along with the increasing dysplasia degree of colorectal tubular adenoma (P < 0.05). Coexpression of JNK1, Raf-1 and Livin increased gradually in the carcinogenesis of sporadic colorectal tubular adenoma, while positive correlation was found among the expressions of JNK1, Raf-1 and Livin.
JNK1, Raf-1 and Livin may be involved in the carcinogenesis of sporadic colorectal tubular adenoma.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 09/2010; 32(9):671-5.
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ABSTRACT: To evaluate the expression of N-cadherin and β-catenin protein and their relationship with clinicopathological characteristics of osteosarcoma.
The expressions of N-cadherin and β-catenin at protein level were detected by immunohistochemical staining in 54 cases of osteosarcoma, 11 cases of osteoid osteoma, 7 cases of osteoblastoma and 8 cases of newly formed bone in nonmalignant bone diseases. The relationship between the two indexes and clinicopathological characteristics of osteosarcoma was analyzed.
In newly formed bone, osteoblastoma, osteoid osteoma and osteosarcoma, the positive expression rate of N-cadherin protein was 75.0%, 71.4%, 63.6% and 35.2%, respectively. The positive expression rate of N-cadherin protein in osteosarcoma was significantly lower than that in osteoid osteoma, osteoblastoma and newly formed bone in nonmalignant bone diseases (P = 0.035). The positive expression rate of N-cadherin protein in osteosarcoma cases with pulmonary metastasis was lower than that in cases without (21.7% vs. 56.3%, P = 0.027). The positive expression rate of N-cadherin protein in osteosarcoma cases died in two years was lower than that in cases lived for more than two years (18.2% vs. 50.0%, P = 0.024). In newly formed bone, osteoblastoma, osteoid osteoma and osteosarcoma, the aberrant expression rate of β-catenin protein was 12.5%, 28.6%, 27.3% and 66.7%, respectively. The aberrant expression rate of β-catenin protein in osteosarcoma was significantly higher than that in osteoid osteoma, osteoblastoma and newly formed bone (P = 0.002). Aberrant expression rate of β-catenin in osteosarcoma cases with pulmonary metastasis was higher than that without (82.6% vs. 43.8%, P = 0.011). An inverse correlation was found between the aberrant expression of β-catenin and N-cadherin expression in osteosarcoma(r = -0.302, P = 0.027).
The positive expression rate of N-cadherin is decreased in osteosarcoma while aberrant expression rate of β-catenin increased. The expression of N-cadherin protein is closely correlated with the metastasis and prognosis of osteosarcoma, but the expression of β-catenin protein is merely correlated with the metastasis of osteosarcoma.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 08/2010; 32(8):586-9.
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ABSTRACT: To construct the human TAP1 expression vector and to evaluate its effects on HLA-I expression in GES-1 cells in vitro.
The human TAP1 expression vector (pcDNA3.1/V5-His-TAP1) was constructed by gene recombination technology. The expression of HLA-I on human gastric epithelial cell line (GES-1 cells) after transfection was detected by RT-PCR, Western blot and flow cytometry (FCM).
Human full-length TAP1 gene was obtained from human peripheral blood mononuclear cells by RT-PCR reaction, then TAP1 gene was inserted into pcDNA3.1/V5-HisB vector to get the TAP1 expression vector (pcDNA3.1/V5-His-TAP1) by recombination technology including digestion with restriction enzymes, ligation and transformation. The vector was sequenced to ensure the sequence fidelity.To further evaluate the function of the TAP1 plasmid we constructed, GES-1 cells were selected as the target cell to be transfected. Firstly RT-PCR and Western blot results showed that the expression of TAP in GES-1 cells was increased after pcDNA3.1/V5-His-TAP1 transfection. Based on the high efficiency of transfection in GES-1 cell, we then detected the expression of HLA-I. The results showed that the expressions of HLA-A, HLA-B and HLA-C at mRNA level were all increased by TAP1 transfection, but no change was found in beta2m mRNA. HLA-I protein level was increased correspondingly with the TAP expression in cells by FCM and Western blot assay.
The TAP1 expression vector was successfully constructed, and it can induce the expression of HLA-I on the GES-1 cells after TAP1 transfection. The results confirm that the TAP1 plays a cruical role in the HLA-I antigen expression and antigen presentation pathway.
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 04/2010; 26(4):329-32.
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The Breast Journal 11/2009; 16(1):105-7. · 1.64 Impact Factor
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Zhonghua bing li xue za zhi Chinese journal of pathology 03/2009; 38(2):136-8.
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ABSTRACT: Both RhoA and Ezrin are confirmed to play an important role in the development and metastasis of tumors. However, the mechanism remains unclear. This study rudimentally investigates the regulatory effect of RhoA on the expression of Ezrin.
After MDA-MB-231 cells were treated with epidermal growth factor (EGF) or following pretreatment of fasudil (the special inhibitor of RhoA), the expression of RhoA, p-RhoA and Ezrin in MDA-MB-231 cells was detected by western blot.
Stimulation of EGF triggered RhoA phosphorylation in MDA-MB-231 cells which reached the maximum at 30 min; RhoA expression did not change; Ezrin expression was enhanced and reached the maximum at 24 h. However, pretreatment of fasudil before EGF stimulation decreased RhoA phosphorylation and Ezrin expression in MDA-MB-231 cells by 72.73% and 51.28%, respectively.
RhoA may regulate the invasion and metastasis of breast cancer cells as an upstream signaling of Ezrin.
Ai zheng = Aizheng = Chinese journal of cancer 03/2009; 28(2):108-11.
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ABSTRACT: To analyze the changing trends of frequency and localization of gastric cancers arising from the gastric cardia, corpus and antrum during the past 14 years in population of the high incidence area of esophageal and gastric carcinoma in Hebei province, China.
The clinicopathological data of 4334 cases of gastric carcinomas among the local residents of Cixian and Zanhuang counties, initially diagnosed in our department from 1993 to 2006, were retrospectively analyzed. The proportion of gastric carcinomas arising from the gastric cardia, corpus and antrum in different years and in patients with different sex and ages were analyzed and compared, and the changing trends of the frequency of gastric carcinoma arising from different sites of the stomach were statistically analyzed.
Among all the 4334 gastric carcinomas, gastric cardia carcinoma accounted for 68.0%, significantly higher than that of corpus (24.2%) and antrum (7.9%; chi(2) = 124.396, P < 0.0001). An increasing tendency in the proportion of gastric cardia carcinoma from 1993 to 2006 was seen. The percentage of cardiac carcinoma in the high incidence area of esophageal carcinoma (Cixian county) was higher than that in the high incidence area of gastric cancer (Zanhuang county) (71.2% vs. 51.2%; chi(2) = 109.648, P < 0.0001). The increase in the incidence of cardiac carcinoma in Cixian county was mainly due to the increase of cardiac carcinoma from 1993 to 2006, while the contributing factor for the increase in the proportion of cardiac carcinomas was resulted from the decrease of incidence of antrum carcinoma in Zanhuang county during the same period. The occurring site of gastric carcinoma was related with age of patients (chi(2) = 58.380, P < 0.0001). The percentage of carcinoma of the gastric body was highest in < 50 year age group, while that in the gastric cardia was highest in 61 - 70 year age group (71.6%).
The major occurring site of gastric carcinoma is the gastric cardia among the local residents in population of the high incidence areas of esophageal and gastric carcinomas during the past 14 years in Hebei province, China. The increasing trend of cardiac carcinoma and decreasing trend of corpus carcinoma in Cixian county and antrum carcinoma in Zanhuang county will be maintained in the coming years if the epidemiological conditions will not be changed.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 12/2008; 30(11):817-20.
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ABSTRACT: To investigate the relationship of ezrin protein expression to the carcinogenesis and prognosis of infiltrating breast ductal carcinoma.
S-P immunohistochemical staining was used to detect the ezrin protein expression in 88 patients with infiltrating ductal carcinoma, and in 54 patients with intraductal hyperplastic lesions of the breast. The clinicopathological data and follow-up information of these patients were all obtained. The relationship of ezrin protein expression to the clinicopathological parameters and the prognostic significance in the infiltrating breast ductal carcinoma was analyzed using Chi-square test (chi2), Kaplan-Meier and Cox models.
The immunohistochemical staining results showed that the strong positive expression rate of ezrin protein in the normal ductal epithelium, simple ductal hyperplasia, atypical hyperplasia and infiltrating ductal carcinoma of the breast was 9.1%, 16.7%, 43.3% and 64.8%, respectively, which was significantly higher in atypical hyperplasia and infiltrating ductal carcinoma than that in the normal ductal epithelium and simple ductal hyperplasia (P < 0.05). The strong ezrin protein expression in the infiltrating ductal carcinoma was positively correlated with axillary lymph node metastasis, histological differentiation grade, TNM stage and CD44v6 expression, but negatively correlated with the expression of E-cadherin (P < 0.05). It was also found that the survival of the patient with strong positive expression of ezrin protein was significantly shorter than that of the control (P < 0.05).
Ezrin protein may play an important role in the carcinogenesis of infiltrating breast ductal carcinoma. The strong expression of ezrin protein may be used as a biomarker for predicting poor prognosis in the patients with infiltrating breast ductal carcinoma.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 05/2008; 30(4):279-83.
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ABSTRACT: To study the effects of Fumonisin B1(FB1) on HLA-I on human peripheral blood mononuclear cells (PBMC) in vitro.
The expression of HLA-I on PBMC by FB1 pretreatment at different dosage(10, 50 micromol/L) was detected with flow cytometry (FCM), Western blot, and semi-RT-PCR, respectively.
The expression of HLA-I on PBMC in vitro at the two experimental concentration was both lower than that of the control after FB1 treatment for 24 h as represented by fluorescence intensity by FCM analysis. Western blot results further confirmed the above results. At mRNA level, HLA-A, B and C mRNA were detected by RT-PCR, and the results showed that no changes were found on the expression of HLA-A, B mRNA between FB1 treated group and the control group, but HLA-C mRNA was inhibited in FB1 treated groups.
10 and 50 micromol/L FB1 could inhibit the expression of HLA-I on human PBMC in vitro at 24 h treatment.
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 10/2007; 23(9):794-6.
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ABSTRACT: To investigate the possible role of STAT3 and p38 in the carcinogenesis of sporadic colorectal tubular adenoma.
The expression of STAT3 and p38 at protein level was studied in 107 sporadic colorectal tubular adenomas with different dysplasia (SCTA-D) or with cancerous changes (SCTA-Ca) by immunohistochemical staining method, meanwhile the expression of STAT3 at mRNA level was detected by in situ hybridization.
Immunohistochemical staining results showed that the positive expression rate of STAT3 and p38 was 12.0%, 59.0%, 91.7% and 8.0%, 47.0%, 91.7% in normal colorectal mucosa (NCM), SCTA-D and SCTA-Ca, respectively, with a statistically significant difference of STAT3 and p38 expression among the SCTA-D, SCTA-Ca and NCM (P < 0.05). The expression of STAT3 and p38 was positively correlated with the degree of dysplasia from mild to severe SCTA-D (P < 0.05). In situ hybridization results showed that the positive expression rate of STAT3 at mRNA level in NCM, SCTA-D and SCTA-Ca was 8.00%, 51.8% and 100.0%, respectively, with a statistically significant difference among these either (P < 0.05). The positive expression of STAT3 at mRNA level was not only positively correlated with the degree of dysplasia (P < 0.05), but also with the expression of p38 (P < 0.05).
STAT3 and p38 may be involved in the carcinogenesis of sporadic colorectal tubular adenoma.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 08/2007; 29(7):514-7.
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Zhonghua bing li xue za zhi Chinese journal of pathology 05/2007; 36(4):265-6.
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ABSTRACT: Matrix metalloproteinases (MMPs) are key enzymes involved in tumor development, invasion and metastasis. The single nucleotide polymorphisms (SNPs) in the promoter regions of MMP genes may influence tumor development and progression via modulating mRNA transcription and protein expression. This study was to explore the correlations of the promoter SNPs in MMP-3 and MMP-7 genes to susceptibility to brain astrocytoma.
The genotype of MMP-3 -1171 5A/6A and MMP-7 -181A/G polymorphisms in 236 patients with brain astrocytoma and 366 healthy controls was detected by polymerase chain reaction-restrictive fragment length polymorphism (PCR-RFLP).
The allelotype and overall genotype distribution of MMP-3 SNP among the astrocytoma patients and healthy controls were similar (P>0.05). Stratified by sex, age, and histological grade, the susceptibility to brain astrocytoma among the subjects with 5A/5A and 5A/6A genotypes and the subjects with 6A/6A genotype were similar(P>0.05). The overall genotype distribution of MMP-7 SNP among the astrocytoma patients and healthy controls were significantly different (P = 0.001). Compared with the A/A genotype, both the G/G and the A/G genotypes significantly increased the susceptibility to astrocytoma [sex-and age-adjusted odds ratio (OR) = 2.77 and 1.69, 95% confidence interval (CI)=1.27-6.02 and 1.01-2.84, respectively]. Stratification analysis showed that the G/G genotype significantly increased the susceptibility to astrocytoma in men (adjusted OR = 3.24, 95% CI = 1.12-9.41) and in the individuals younger than 45 years (adjusted OR = 3.16, 95% CI = 1.09-9.16). When stratified by histological grade, the A/G genotype increased the susceptibility to grade II astrocytoma by about 2 folds (adjusted OR = 2.06, 95% CI = 1.05 - 4.05), while the G/G genotype increased the susceptibility to grade II-IV astrocytoma by about 3 folds.
MMP-7 -181A/G polymorphism may influence the susceptibility to astrocytoma, while MMP-3-1171 5A/6A polymorphism has no correlation to the susceptibility.
Ai zheng = Aizheng = Chinese journal of cancer 05/2007; 26(5):463-8.
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ABSTRACT: To explore the effects of Vitamin C (Vit C) on the apoptosis and proliferation inhibition of human peripheral blood mononuclear cells (HPBMCs) induced by deoxynivalenol (DON) in vitro.
The effects of Vit C pretreatment at different dosages (25 micromol/L and 100 micromol/L) on apoptosis, apoptosis related genes expression and proliferation inhibition of HPBMCs induced by DON were evaluated with cell culture, flow cytometric DNA analysis and Western blotting.
Flow cytometry (FCM) analysis showed that the apoptosis rate of HPBMCs in 2000 microg/L DON group was (28.82 +/- 1.67)%, which was significantly higher than that in control group (14.07 +/- 0.70, P < 0.05). Compared with DON group, the apoptosis rate of HPBMCs in 25 micromol/L Vit C pretreatment group was significantly decreased (28.82 +/- 1.67)% vs (22.39 +/- 1.05)%, P < 0.05, while that in 100 micromol/L Vit C pretreatment group was obviously increased (36.07 +/- 2.92)%, P < 0.05. Western blotting analysis showed that the expression of Bax and Caspase-3 up-regulated by DON was markedly decreased, while the expression of Bcl-2 down-regulated by DON was increased by 25 micromol/L Vit C pretreatment (P < 0.05). 100 micromol/L Vit C pretreatment could further increase the expression of Bax and Caspase-3 of HPBMCs induced by DON, while no significant effects on the Bcl-2 expression induced by DON were seen. FCM analysis showed that the proliferation index of HPBMCs in Vit C pretreatment groups at different dosages was all dramatically increased as compared with that in DON groups (P < 0.05).
25 micromol/L Vit C pretreatment could at certain extent inhibit the apoptosis and reverse the abnormal expression of apoptosis related genes of HPBMCs induced by DON in vitro, while 100 micromol/L Vit C pretreatment could further increase the apoptosis rate of HPBMCs induced by DON. Vit C pretreatment could reverse the proliferation inhibition of HPBMCs induced by DON in vitro.
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] 10/2006; 40(5):309-13.
