Publications (23)27.44 Total impact
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Article: Folate metabolism gene polymorphisms MTHFR C677T and A1298C and risk for Down syndrome offspring: a meta-analysis.
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ABSTRACT: OBJECTIVES: MTHFR C677T and A1298C have been associated with the risk of having an infant with Down syndrome (DS), but results were conflicting. We performed this meta-analysis to derive a more precise estimation of the association between maternal MTHFR polymorphisms and DS. STUDY DESIGN: An electronic search of PubMed and Chinese Biomedicine database was conducted to select studies for meta-analysis. Twenty-eight case-control studies containing MTHFR C677T and A1298C gene polymorphisms were chosen, and odds ratio (OR) with confidence interval (CI) was used to assess the strength of this association. RESULTS: Case-control studies including 2806 cases and 4597controls for MTHFR C677T were identified. The overall results suggested that the variant genotypes MTHFR C677T were associated with DS risk (TT+CT vs. CC: OR=1.305, 95% CI: 0.125-1.514, p=0). In the stratified analysis, individuals with the T-carriers genotype in the dominant model had increased risk of DS (OR=1.171, 95% CI: 0.976-1.405, p=0.09) in Caucasian subjects and in Asian subjects (OR=1.749, 95% CI: 1.084-2.824, p=0.022). In addition, case-control studies including 1854 cases and 2364 controls for MTHFR A1298C were chosen. Associations between MTHFR A1298C and the risk of having a child with DS were not found. A symmetric funnel plot, the Egger's test (p=0.126) suggested a lack of publication bias. CONCLUSION: This meta-analysis supports the idea that MTHFR C677T genotype is associated with increased risk for DS offspring.European journal of obstetrics, gynecology, and reproductive biology 01/2013; · 1.97 Impact Factor -
Article: [The regulation of anoikis in tumor invasion and metastasis].
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ABSTRACT: As a barrier to metastasis of cancer, cells that lost contact with the neighbouring cells or extracellular matrix(Extracellular matrix, ECM) will be subjected to apoptosis. This cell death process has been termed "anoikis". When normal epithelial cells or solid tumor cells without metastatic potential detach from the primary site, and then enter into the circulatory system, the anoikis mechanism will be activated. The significance of anoikis is to prevent the shedding cells from growing and implanting into other inappropriate sites. Tumor cells, especially several malignant cells that is prone to transfer to distant sites, have properties of anti-anoikis, which facilitates metastasis as well as invasion of tumor cells. The studies found that tumor cells can resist anoikis through multiple mechanisms: the pro-survival pathways are activated by cells autocrine growth factors and paracrine factors derived from neighboring cells; cells change the pattern of integrin expression so that they can receive survival signals from new environment; reactive oxygen species (ROS) activates growth factor receptors in a ligand-independent way to avoid apoptosis; and epithelial-mesenchymal transformation(EMT) is activated etc.. All of these mechanisms lead to activation of survival signals and inhibition of apoptotic pathways, and ultimately cause resistance to anoikis as well as metastasis. This paper summarizes the key mechanisms of the current studies on metastasis, which also suggest important targets for cancer therapy.Hereditas (Beijing) 01/2013; 35(1):10-6. -
Article: [The cooperation between p53 and Ras in tumorigenesis.]
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ABSTRACT: Inactivation of the tumor suppressor gene and activation of the oncogene cooperate to promote the multistep process of tumorigenesis. p53 is considered to be the most important tumor suppressor gene. p53 is usually found as a result of somatic missense mutation in approximately 50% of human cancers. Ras is found to be one of the most frequently mutated oncogenes in human tumors with the reported frequencies ranging from 30% to 90%. It has been found in many studies synergistic effect between tumor suppressor p53 and oncogene Ras occurs during the multistep process of tumorigenesis. According to the current reports, the cooperative effect between p53 and Ras can be divided into three types: the regulation of p53 for Ras function, , the regulation of Ras for p53, and the cooperation between p53 and Ras to control critical genes that are closely related to tumorigenesis. Understanding their synergistic effects will not only help us further disclose mechanism of tumorigenesis caused by p53 inactivation and Ras activation, but also facilitate personalized treatments and pharmacological target selection for cancer therapy. Therefore, we reviewed the recent progress of synergistic effect be-tween p53 and Ras and its role in tumorigenesis.Hereditas (Beijing) 12/2012; 34(12):1513-1521. -
Article: Association Between the CTLA-4 +49A/G Polymorphism and Type 1 Diabetes: A Meta-Analysis.
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ABSTRACT: Background:+49A/G polymorphism of the cytotoxic T-lymphocyte-associated antigen-4 gene (CTLA-4) has been associated with type 1 diabetes (T1D). However, results were inconsistent. The aim of this study was to quantitatively summarize the evidence for CTLA-4 +49A/G polymorphism and T1D. Methods: Electronic search of PubMed was conducted to select studies. Case-control studies containing available genotype frequencies of CTLA-4 +49 were chosen, and the odds ratio (OR) with 95% confidence interval (CI) was used to assess the strength of this association. Results: 49 case-control studies, including 8976 cases and 11012 controls, were identified. 8 studies were eliminated from the total 49 studies because of p<0.05 (p value for Hardy-Weinberg equilibrium in the control group) in these studies, which induce significant publication bias. The overall results suggested that the variant genotypes were highly associated (p<0.01) with T1D risk in all genetic models (additive model: OR 1.345, 95% CI 1.249-1.448, p<0.001; recessive model: OR 1.530, 95% CI 1.370-1.708, p<0.001; dominant model: OR 1.409, 95% CI 1.263-1.572 p<0.001). Similarly, in subgroup analyses for ethnicity (Caucasian, Asian), the results were positive. Conclusion: This meta-analysis suggests that the CTLA-4 +49A/G polymorphism is highly associated (p<0.01) with increased risk of T1D, especially in Caucasians and Asians. To validate this association, further studies with more participants worldwide are needed to examine associations between this polymorphism and T1D. Otherwise, we found that the studies of Africans are rare. More studies in Africans are needed especially.Genetic Testing and Molecular Biomarkers 09/2012; · 1.11 Impact Factor -
Article: Association between the CTLA-4 +49A/G polymorphism and Graves' disease: A meta-analysis.
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ABSTRACT: The +49A/G polymorphism of the cytotoxic T-lymphocyte-associated antigen-4 gene (CTLA-4) has been associated with Graves' disease (GD). However, results have been inconsistent. The aim of this study was to quantitatively summarize the evidence for CTLA-4 +49A/G polymorphism and GD. Electronic search of PubMed was conducted to select studies. Case-control studies containing available genotype frequencies of CTLA-4 +49 were chosen, and Odds ratio (OR) with 95% confidence interval (CI) was used to assess the strength of this association. Forty-two case-control studies including 8,288 cases and 9,372 controls were identified. Three studies were eliminated from the total 42 studies due to a p-value <0.05 (p-value for Hardy-Weinberg equilibrium in control group) in these studies which induced significant publication bias. The overall results suggested that the variant genotypes were highly associated (p<0.01) with GD risk in all genetic models (additive model: OR, 1.443; 95% CI, 1.319-1.578; p<0.001; recessive model: OR, 1.589; 95% CI, 1.396-1.808; p<0.001; dominant model: OR, 1.621; 95% CI, 1.430-1.837; p<0.001). Similarly, in the subgroup analyses for ethnicity (Caucasian, Asian), the results were positive. This meta-analysis suggests that the CTLA-4 +49A/G polymorphism is highly associated (p<0.01) with increased risk of GD, especially in Caucasians and Asians. To validate this association, further studies with larger participants worldwide are needed to examine associations between this polymorphism and GD.Experimental and therapeutic medicine 09/2012; 4(3):538-544. -
Article: Association between the CTGF -945C/G polymorphism and systemic sclerosis: A meta-analysis.
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ABSTRACT: BACKGROUND: The -945C/G polymorphism of the connective tissue growth factor (CTGF) has been associated with systemic sclerosis, however, results were conflicted. The aim of this study was to validate the evidence for the CTGF -945C/G polymorphism and systemic sclerosis risk. METHODS: Electronic search of PubMed was conducted to select studies. Case-control studies containing available genotype frequencies of -945C/G were chosen, and odds ratio (OR) with 95% confidence interval (CI) was used to assess the strength of this association. RESULTS: Six published case-control studies including 3335 cases and 3589 controls were identified. The overall results suggested that the variant genotypes were not associated with the systemic sclerosis risk (OR=0.947, 95% CI: 0.792-1.132, p=0.55). The stratified analysis in Caucasian (OR=1.002, 95% CI: 0.837-1.2, p=0.788) did not suggest an association either. However, analysis in Asian (OR=0.632, 95% CI: 0.459-0.869, p=0.005) showed that CC/CG genotype greatly decreased the susceptibility of systemic sclerosis in a dominant model. Asymmetric funnel plot, the Egger's test (p=0.292), and the Begg's test (p=0.593) were all suggestive of the lack of publication bias. CONCLUSION: This meta-analysis supports that CC/CG genotype greatly decreased the susceptibility of systemic sclerosis in Asian. Due to the limited samples in subpopulations, further prospective studies with larger number of participants worldwide are needed to examine the association between the CTGF -945C/G polymorphism and systemic sclerosis.Gene 08/2012; 509(1):1-6. · 2.34 Impact Factor -
Article: [The new function of p53 family and its pathway related proteins in female reproduction].
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ABSTRACT: p53 is an important tumor suppressor gene and one of the key genes in sensing and regulating responses to the environmental stress. Recent study showed that cold winter temperature naturally selected p53 Arg72 in eastern Asian population, suggesting that p53 plays a role in reproduction. It has also been reported that some SNPs of p53, Mdm2(Murine double minute 2), MdmX and Hausp (Herpes virus-associated ubiquitin-specific protease) in p53 pathway are associated with the risk of the women's reproduction disorder. p53 regulates the LIF (leukaemia inhibitory factor) expression level by its DBD domain, and thus contributes to female reproduction by affecting the embryo implantation process. The MDM2, MDMX, and HAUSP proteins regulates the level and activity of p53 protein, which are critical for the appropriate p53 response in the embryo implantation process. The members of p53 family, p63 and p73, also play roles in female reproduction through other pathways. p63 has been implicated as a major regulator of oocyte death following treatment with irradiation and chemotherapeutic drugs, which prevents fetal malformation. p73 regulates the formation of spindle assembly complex(SAC). The dysfunction of SAC results in poor blastocyst quality and defects in kinetochore-microtubule associations, which leads to aneuploidy. This review summarized the function of p53 family and its pathway related proteins in female reproduction, pointed out a new method in improving the success rate in IVF-ET, and provided a new diagnosis idea for unexplained infertile women. It will facilitate personalized strategies in the infertility therapy.Hereditas (Beijing) 08/2012; 34(8):943-9. -
Article: Two mechanisms underlying the loss of p16(Ink4a) function are associated with distinct tumorigenic consequences for WS MEFs escaping from senescence.
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ABSTRACT: Werner syndrome (WS) mouse embryonic fibroblasts (MEFs) can spontaneously escape from senescence and become immortalized, either tumorigenic or non-tumorigenic. Our data revealed a single p53(N236S) point mutation in the tumorigenic cell lines, which was correlated with the down-regulation of p21(Waf1/Cip1). p16(Ink4a) expression was significantly decreased in all immortalized cell lines. Bisulfate sequencing indicated that the p16(Ink4a) gene was methylated in the tumorigenic cells. Exogenous overexpression of p21(Waf1/Cip1) demethylated p16(Ink4a) and restored its expression, which induced cell growth arrest and senescence. While in non-tumorigenic immortalized cells, the Ink4a loci and adjacent genomic DNA were found to be deleted. These data suggest that the loss of p16(Ink4a) function by either genomic DNA deletion or methylation have been adopted by senescent WS MEFs escaping from senescence, with distinct tumorigenic consequences. The fact that cells that had escaped senescence via the spontaneous biallelic deletion of the Ink4a loci could not form tumors suggests that the functional loss of p16(Ink4a)per se might not be sufficient for tumorigenesis; most likely, it is a byproduct and passenger mutation. The mutations in factors regulating p16(Ink4a) methylation might be the driver mutation. These findings shed light on the strategy of anti-aging by regulating p16(Ink4a) expression.Mechanisms of ageing and development 07/2012; 133(8):549-55. · 4.18 Impact Factor -
Article: Association of p53 Arg72Pro polymorphism with gastric cancer: a meta-analysis.
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ABSTRACT: Background: p53 tumor suppressor gene Arg72Pro polymorphism has been associated with gastric cancer. However, results were inconsistent. We performed this meta-analysis to estimate the association between p53 Arg72Pro polymorphism and gastric cancer. Methods: An electronic search of PubMed was conducted to select studies. Studies containing available genotype frequencies of Arg72Pro were chosen, and the association was assess by pooled odds ratio (ORs) with 95% confidence interval (CIs). Results: The meta-analysis suggested that the p53 Arg72Pro was associated with the gastric cancer risk (Additive model: OR = 1.149, 95% CI = 1.045-1.263, p = 0.004; Dominant model: OR = 1.18, 95% CI = 1.049-1.328, p = 0.006; Recessive model: OR = 1.202, 95% CI = 1.013-1.427, p = 0.035) in Asian subgroup. Conclusion: This meta-analysis suggests that p53 Arg72Pro polymorphism is associated with increased risk of gastric cancer in Asians.Biomarkers 07/2012; 17(7):597-603. · 2.21 Impact Factor -
Article: Note of clarification of data in the meta-analysis of methylenetetrahydrofolate reductase C677T polymorphisms in polycystic ovary syndrome.
Molecular Human Reproduction 06/2012; 18(10):514-5. · 3.85 Impact Factor -
Article: Association between the MTHFR C677T polymorphism and recurrent pregnancy loss: a meta-analysis.
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ABSTRACT: C677T polymorphism of the methylenetetrahydrofolate reductase (MTHFR) has been associated with recurrent pregnancy loss (RPL). However, results were conflicting. The aim of this study was to quantitatively summarize the evidence for MTHFR C677T polymorphism and RPL risk. Electronic search of PubMed and the Chinese Biomedicine database was conducted to select studies. Case-control studies containing available genotype frequencies of C677T were chosen, and odds ratio (OR) with 95% confidence interval (CI) was used to assess the strength of this association. The case-control studies including 2427 cases and 3118 controls were identified. The meta-analysis stratified by ethnicity showed that individuals with the homozygous TT genotype had increased risk of RPL (OR=1.574, 95% CI: 1.163-2.13, p=0.003), in Asians (OR=1.663, 95% CI: 1.012-2.731, p=0.045). Results among Caucasians did not suggest an association (OR=1.269, 95% CI: 0.914-1.761, p=0.155). A symmetric funnel plot, the Egger's test (p=0.285), and the Begg's test (p=0.529) were all suggestive of the lack of publication bias. The studies conducted in each of the defined number of pregnancy losses-two or more pregnancy losses, and three or more pregnancy losses-showed no effect of the C677T polymorphism on RPL except for the TT versus CT+CT genotype comparison for the three or more pregnancy loss subgroup (OR=1.792, 95% CI: 1.187-2.704, p=0.005). This meta-analysis supports the idea that MTHFR C677T genotype is associated with increased risk of RPL, except for Caucasians. To draw comprehensive and true conclusions, further prospective studies with larger numbers of participants worldwide are needed to examine associations between MTHFR C677T polymorphism and RPL.Genetic Testing and Molecular Biomarkers 02/2012; 16(7):806-11. · 1.11 Impact Factor -
Article: [Effects of some extenders and monoamines on sperm cryopreservation in tree shrews (Tupaia belangeri)].
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ABSTRACT: The tree shrew may be an important experimental animal for disease models in humans. The effects of some extenders and momamines on sperm cryopreservation will provide helpful data for experimentation of strains and conservation of genetic resources in tree shrews. Epididymal sperm were surgically harvested from male tree shrews captured around Kunming, China and sperm motility, acrosome integrity and fertility were assessed during cryopreservation. In Experiment 1 eight extenders (TTE, TCG, TCF, TTG, BWW, BTS, DM, and SR) supplemented with 0.4 mol/L DMSO were used to dilute the sperm: only TTE, DM and SR showed no differences in motility and acrosome integrity compared to fresh controls after equilibration. After freezing and thawing, sperm in any extender showed lower motility than fresh control and sperm in DM showed higher motility than other groups. However, BWW produced the lowest motility. For acrosome integrity, TTE and DM showed higher than BWW, BTS and SR after equilibration. The parameter in DM was higher than other groups (except TTE) after thawing. In Experiment 2 four penetrating cryoprotectant agents (CPA) [dimethyl-formamide (DF), formamide (F), dimethylacetamide (DA), and acetamide (A)] at 0.2 mol/L, 0.4 mol/L, 0.8 mol/L, and 1.2 mol/L, respectively were added to the DM extender. Motility showed no difference among CPA groups and non-CPA group (control) after equilibration, but all thawed sperm showed lower values in motility and acrosome integrity than pre-freezing groups. However, sperm in 0.8 mol/L DF and 0.4 mol/L DMSO showed higher values in both parameters than that in other CPA groups (P>0.05). In Experiment 3 the fertilization rate of oocytes inseminated with 0.4mol/L DMSO (50%) were higher than that with 0.8mol/L DF (16%). In conclusion, non-ion extenders supplemented with egg yolk may be better for sperm cryopreservation in tree shrews and cryoprotectant effects of monoamines agents should be further studied in this species.Zoological Research 02/2012; 33(1):19-28. -
Article: Lack of association between p53 codon 72 polymorphism and endometrial cancer: a meta-analysis.
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ABSTRACT: It has been suggested that the p53 tumor suppressor gene Arg72Pro polymorphism is associated with endometrial cancer. However, results have been inconsistent. We performed this meta-analysis to estimate the association between p53 Arg72Pro polymorphism and endometrial cancer. An electronic search of PubMed was conducted to select studies. Studies containing available genotype frequencies of Arg72Pro were chosen, and the association was assessed by pooled odds ratios (ORs) with 95% confidence intervals (CIs). Nine published studies, including 829 endometrial cancer cases and 1387 controls, were identified. The overall results suggested that the variant genotypes were not associated with the endometrial cancer risk in all genetic models (additive model: OR 1.027, 95% CI 0.893-1.18, P=0.71; recessive model: OR 1.099, 95% CI 0.802-1.507, P=0.556; dominant model: OR 1.013, 95% CI 0.842-1.219 P=0.89). Similarly, the results were negative in subgroup analyses for ethnicity (Caucasian, Asian). This meta-analysis suggests that p53 codon 72 polymorphism is not associated with increased risk of endometrial cancer, especially in Caucasians and Asians. To validate the association between this polymorphism and endometrial cancer, further studies with larger numbers of participants worldwide are needed.Cancer epidemiology. 01/2012; 36(3):e153-7. -
Article: p53 codon 72 polymorphism and endometriosis: a meta-analysis.
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ABSTRACT: p53 tumour suppressor gene Arg72Pro polymorphism has been associated with endometriosis. However, the current available data were inconsistent. We performed this meta-analysis to estimate the association between p53 Arg72Pro polymorphism and endometriosis. Electronic screening of PubMed library was conducted to select studies. Studies containing available genotype frequencies of Arg72Pro were chosen, and pooled odds ratio (OR) with 95% confidence interval (CI) was used to assess the association. Six published studies, including 749 endometriosis and 857 controls were identified. The overall results suggested that the variant genotypes were not associated with the endometriosis risk (Pro/Pro + Arg/Pro vs. Arg/Arg: OR = 1.552, 95% CI 0.916-2.632, p = 0.103). In the stratified analysis, individuals carried the Pro allele in a dominant model had increased risk of endometriosis (OR = 2.595, 95% CI 1.005-6.702, p = 0.049) in Asian subjects. The symmetric funnel plot, the Egger's test (p = 0.602), and the Begg's test (p = 0.167) were all suggestive of the lack of publication bias. However, the association was not significant between this polymorphism and endometriosis in Caucasian (OR = 1.005, 95% CI 0.755-1.337, p = 0.972). This meta-analysis suggests that p53 codon 72 Pro/Pro + Arg/Pro genotypes are associated with increased risk of endometriosis in Asian. To validate the association between p53 codon 72 polymorphism and endometriosis, further studies with larger participants worldwide are needed.Archives of Gynecology 01/2012; 285(6):1657-61. · 0.91 Impact Factor -
Article: The gain of function of p53 mutant p53S in promoting tumorigenesis by cross-talking with H-RasV12.
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ABSTRACT: The loss of wild type p53 tumor suppressive function and oncogenic gain-of-function of p53 mutants have been showing important implications in tumorigenesis. The p53(N236S) (p53(N239S) in human, p53S) mutation has been shown to lose wild type p53 function by yeast assay. However, its gain of function is still not clear. By gel shift assay, we showed that mutant p53S had lost its DNA binding ability to its target promoters. Further real-time PCR data confirmed that p53S had lost the function of regulating the transcription of p21( Cip1/Waf1), cyclin G, PUMA, and Bax in response to 10Gy irradiation. These data confirmed the loss of function of p53S in mammalian cells. By xenograft assay, we showed that the p53S per se was not oncogenic enough to form tumor, however, cooperating with H-RasV12, p53S could dramatically promote tumorigenesis in p53 null MEFs. Further study showed that co-expression of p53S and H-RasV12 could increase the expression level of H-RasV12 and partially eliminate the elevation of stress response proteins such as Chk2, γ-H2AX, Hsp70, Rb, p16(Ink4a) caused by either p53S or H-RasV12. These data suggested that p53S cross-talked with H-RasV12 and reduced the cellular stress response to oncogenic signals, which facilitated the cell growth and tumorigenesis. Together these data provided the molecular basis for the cooperation of p53S and H-RasV12 and revealed the gain of function of p53S in cross-talking with H-RasV12. This study revealed an important aspect of gain of function for p53 mutant, therefore might shed light on the clinical strategy in targeting p53 mutant.International journal of biological sciences 01/2012; 8(5):596-605. · 2.70 Impact Factor -
Article: Loss of p16(Ink4a) Function Rescues Cellular Senescence Induced by Telomere Dysfunction.
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ABSTRACT: p16(Ink4a) is a tumor suppressor and a marker for cellular senescence. Previous studies have shown that p16(Ink4a) plays an important role in the response to DNA damage signals caused by telomere dysfunction. In this study, we crossed Wrn(-/-) and p16(Ink4a-/-) mice to knock out the p16(Ink4a) function in a Wrn null background. Growth curves showed that loss of p16(Ink4a) could rescue the growth barriers that are observed in Wrn(-/-) mouse embryonic fibroblasts (MEFs). By challenging the MEFs with the global genotoxin doxorubicin, we showed that loss of p16(Ink4a) did not dramatically affect the global DNA damage response of Wrn(-/-) MEFs induced by doxorubicin. However, in response to telomere dysfunction initiated by the telomere damaging protein TRF2(ΔBΔM), loss of p16(Ink4a) could partially overcome the DNA damage response by disabling p16(Ink4a) up-regulation and reducing the accumulation of γ-H2AX that is observed in Wrn(-/-) MEFs. Furthermore, in response to TRF2(ΔBΔM) overexpression, Wrn(-/-) MEFs senesced within several passages. In contrast, p16(Ink4a-/-) and p16(Ink4a-/-)Wrn(-/-) MEFs could continuously grow and lose expression of the exogenous TRF2(ΔBΔM) in their late passages. In summary, our data suggest that in the context of telomere dysfunction, loss of p16(Ink4a) function could prevent cells from senescence. These results shed light on the anti-aging strategy through regulation of p16(Ink4a) expression.International Journal of Molecular Sciences 01/2012; 13(5):5866-77. · 2.60 Impact Factor -
Article: p53 codon 72 polymorphism and recurrent pregnancy loss: a meta-analysis.
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ABSTRACT: Arg72Pro polymorphism of the p53 tumour suppressor gene have been associated with recurrent pregnancy loss. However, results were inconsistent. We performed this metaanalysis to drive amore precise estimation of association between p53 codon 72 polymorphism and recurrent pregnancy loss. Electronic searche of PubMed was conducted to select studies. Case-control studies containing available genotype frequencies of Arg72Pro were chose, and Odds ratio (OR) with 95% confidence interval (CI) was used to assess the strength of this association. 4 case-control studies including 523 cases and 378controls were identified. This meta-analysis showed that individuals with the homozygous Pro/Pro genotype had increased risk of recurrent pregnancy loss (OR = 1.85, 95% CI: 1.078 ~ 3.173, p = 0.025) in the pooled analyses. An symmetric funnel plot, the Egger's test (P = 0.497), and the Begg- test (P = 0.85) were all suggestive of the lack of publication bias. This meta-analysis supports the idea that p53 condon72 Pro/Pro genotype is associated with increased risk of recurrent pregnancy loss. To draw comprehensive and true conclusions, further prospective studies with larger numbers of participants worldwide are needed to examine associations between p53 codon 72 polymorphism and recurrent pregnancy loss.Journal of Assisted Reproduction and Genetics 08/2011; 28(10):965-9. · 1.84 Impact Factor -
Article: [Recent advances in mutant p53 and novel personalized strategies for cancer therapy].
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ABSTRACT: Protein p53 is the most intensively studied tumor suppressor protein. Recent studies keep revealing its new function in metabolism and reproduction. At the same time, it is also found that varieties of p53 mutant gained new function in promoting tumorigenesis. These studies provide the basis for understanding the personalized gain of function of p53 mu-tants and help us searching for the new strategies for reactivation of wild-type p53 and correction of the function of p53 mutants. The personalized treatment targeting different p53 mutants will be the focus for cancer treatment. Here, we re-viewed the discovered gain of function of some p53 mutants and the molecular strategies for reactivating wild type p53 function: by use of small molecules or polypeptides to reactivate the wild type function of p53 mutants in tumor cells; by exogenous expression of wild type p53 carried by recombinant adenovirus in tumor cells; and by inhibition the interaction between p53 and mdm2 to stabilize wild type p53 proteins. Further study of variety of p53 point mutations farcilitates de-signing more effectively personalized strategies in the cancer therapy.Hereditas (Beijing) 06/2011; 33(6):539-48. -
Article: Pu-erh Tea Inhibits Tumor Cell Growth by Down-Regulating Mutant p53.
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ABSTRACT: Pu-erh tea is a kind of fermented tea with the incorporation of microorganisms' metabolites. Unlike green tea, the chemical characteristics and bioactivities of Pu-erh tea are still not well understood. Using water extracts of Pu-erh tea, we analyzed the tumor cell growth inhibition activities on several genetically engineered mouse tumor cell lines. We found that at the concentration that did not affect wild type mouse embryo fibroblasts (MEFs) growth, Pu-erh tea extracts could inhibit tumor cell growth by down-regulated S phase and cause G1 or G2 arrest. Further study showed that Pu-erh tea extracts down-regulated the expression of mutant p53 in tumor cells at the protein level as well as mRNA level. The same concentration of Pu-erh tea solution did not cause p53 stabilization or activation of its downstream pathways in wild type cells. We also found that Pu-erh tea treatment could slightly down-regulate both HSP70 and HSP90 protein levels in tumor cells. These data revealed the action of Pu-erh tea on tumor cells and provided the possible mechanism for Pu-erh tea action, which explained its selectivity in inhibiting tumor cells without affecting wild type cells. Our data sheds light on the application of Pu-erh tea as an anti-tumor agent with low side effects.International Journal of Molecular Sciences 01/2011; 12(11):7581-93. · 2.60 Impact Factor -
Article: [Whole genome amplification and its application in forensic individual identification].
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ABSTRACT: Whole genome amplification (WGA) is a technique that could non-selectively amplify the genomic DNA. In recent years, intensive studies have been made on application of WGA in trace DNA amplification, which might be applied to amplify trace DNA collected from crime scenes and provide enough DNA templates for forensic individual identification. However, the problem of amplification bias happened in the complicated test materials from real crime scenes is still troublesome. Development of WGA method with low amplification bias and high yield is the main target of current forensic research. Here, we reviewed the advances and the application prospect of WGA in individual identification. This might provide a reference for solving the problem of the amplification bias.Hereditas (Beijing) 11/2010; 32(11):1119-25.
Top co-authors
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Institutions
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2009–2013
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Kunming University of Science and Technology
Kunming, Yunnan, China
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2012
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Kunming Institute of Zoology CAS
Kunming, Yunnan, China
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