Assessment of fragile histidine triad expression in ameloblastoma, odontogenic keratocyst and dentigerous cyst

Background: FHIT (Fragile histidine triad) a member of tumor suppressor family, has been extensively studied in many solid tumors including head and neck squamous cell carcinoma. Among all head and neck cyst and tumors odontogenic lesions account approximately 3%-9%. The molecular pathogenesis of these lesions is less explored. Defects in cell cycle regulators and tumor suppressor genes could result in the development of odontogenic cyst and tumors. Hence, we aimed to determine the significant role of a tumor suppressor gene FHIT in most commonly occurring odontogenic lesions mainly ameloblastoma, odontogenic keratocyst and dentigerous cyst. Subjects and Methods: Immunohistochemical analysis of FHIT was done in ameloblastoma, odontogenic keratocyst, dentigerous cyst and dental follicle. Interpretation of the stained slides were done using standard scoring criteria by two pathologist. The results were subjected for statistical analysis. Results: Expression of FHIT varied among the groups, with highest negative expression in ameloblastoma 44.4% followed by odontogenic keratocyst 14% and 100%positive expression was seen in dentigerous cyst. The expression levels between the groups were statistically insignificant. Conclusion: The varied expression or negative expression of FHIT could be considered as an indicator for aggressive behavior and transformation of preneoplastic/cystic epithelium.

Interaction between abnormal expression of fragile histidine triad and methyl-CpG-binding protein 2 on cervical cancerization / 中华流行病学杂志

Objective To explore the relationship between abnormal expression of fragile histidine triad (FHIT) gene and methyl-CpG-binding protein 2 (MeCP2) as well as their interaction on cervical cancerization.Methods A total of 73 patients with cervical squamous cell carcinoma (SCC),113 patients with cervical intraepithelial neoplasia (CIN Ⅰ,n =45;CIN Ⅱ/Ⅲ,n=68) and 60 women with normal cervix (NC) were included in the study.Real time PCR and Western blot were performed to detect the expression levels of mRNA and protein about FHIT and MeCP2,respectively.The methylation status of FHIT gene CpG island was tested by methylation-specifc PCR (MSP).Kruskal-Wallis H test,x2 test,trend x2 test and Spearman correlation analysis were conducted with software SPSS 20.0.The interaction was evaluated by generalized multifactor dimensionality reduction (GMDR) model.Results With the deterioration of cervical lesion,the methylation rates of FHIT gene CpG island (x2=18.64,P＜0.001;trendx2=18.08,P＜0.001) increased gradually,while the expression levels of FHIT mRNA (H=27.32,P＜0.001;trendx2=12.65,P＜0.001) and protein (H=47.10,P＜0.001;trendx2=29.79,P＜0.001) decreased gradually.There was a negative correlation between the methylation rates of FHIT gene CpG island and the expression level of FHIT protein (r=-0.226,P＜0.001).The levels of MeCP2 mRNA (H=26.19,P＜0.001;trend x2=11.81,P=0.001) and protein (H=69.02,P＜ 0.001;trend x2 =47.44,P＜ 0.001) increased gradually with the aggravation of cervical lesions.There was a positive correlation between the expression level of MeCP2 protein and the FHIT mRNA Ct ratio (r=0.254,P＜0.001).Expression of proteins were negatively correlated between MeCP2 and FHIT (r=-0.213,P=0.001).The results analyzed by GMDR model showed that there were interactions among high MeCP2 protein expression,the CpG island methylation of FHIT and mRNA and protein expression in CIN Ⅱ/Ⅲ group,and among high MeCP2 mRNA and protein expression,the CpG island methylation of FHIT and low mRNA and protein expression in SCC group.Conclusion High expression of MeCP2 mRNA and protein,the CpG island methylation and low mRNA and protein expression of FHIT could increase the risk of cervical carcinogenesis,and there might be a synergistic effect on cervical carcinogenesis.

Interaction between abnormal expression of fragile histidine triad and methyl-CpG-binding protein 2 on cervical cancerization / 中华流行病学杂志

Objective To explore the relationship between abnormal expression of fragile histidine triad (FHIT) gene and methyl-CpG-binding protein 2 (MeCP2) as well as their interaction on cervical cancerization.Methods A total of 73 patients with cervical squamous cell carcinoma (SCC),113 patients with cervical intraepithelial neoplasia (CIN Ⅰ,n =45;CIN Ⅱ/Ⅲ,n=68) and 60 women with normal cervix (NC) were included in the study.Real time PCR and Western blot were performed to detect the expression levels of mRNA and protein about FHIT and MeCP2,respectively.The methylation status of FHIT gene CpG island was tested by methylation-specifc PCR (MSP).Kruskal-Wallis H test,x2 test,trend x2 test and Spearman correlation analysis were conducted with software SPSS 20.0.The interaction was evaluated by generalized multifactor dimensionality reduction (GMDR) model.Results With the deterioration of cervical lesion,the methylation rates of FHIT gene CpG island (x2=18.64,P＜0.001;trendx2=18.08,P＜0.001) increased gradually,while the expression levels of FHIT mRNA (H=27.32,P＜0.001;trendx2=12.65,P＜0.001) and protein (H=47.10,P＜0.001;trendx2=29.79,P＜0.001) decreased gradually.There was a negative correlation between the methylation rates of FHIT gene CpG island and the expression level of FHIT protein (r=-0.226,P＜0.001).The levels of MeCP2 mRNA (H=26.19,P＜0.001;trend x2=11.81,P=0.001) and protein (H=69.02,P＜ 0.001;trend x2 =47.44,P＜ 0.001) increased gradually with the aggravation of cervical lesions.There was a positive correlation between the expression level of MeCP2 protein and the FHIT mRNA Ct ratio (r=0.254,P＜0.001).Expression of proteins were negatively correlated between MeCP2 and FHIT (r=-0.213,P=0.001).The results analyzed by GMDR model showed that there were interactions among high MeCP2 protein expression,the CpG island methylation of FHIT and mRNA and protein expression in CIN Ⅱ/Ⅲ group,and among high MeCP2 mRNA and protein expression,the CpG island methylation of FHIT and low mRNA and protein expression in SCC group.Conclusion High expression of MeCP2 mRNA and protein,the CpG island methylation and low mRNA and protein expression of FHIT could increase the risk of cervical carcinogenesis,and there might be a synergistic effect on cervical carcinogenesis.

Interaction between fragile histidine triad methylation, protein expression and human papillomavirus 16 infection in cervical carcinogenesis / 中华流行病学杂志

Objective To investigate the association between fragile histidine triad (FHIT) gene methylation,abnormal protein expression and HPV16 infection as well as their interactions in cervical carcinogenesis.Methods A total of 108 patients with normal cervical (NC),142 cases of cervical intraepithelial neoplasia (CIN1,n=72;CIN2 +,n=70),and 100 new cases of cervical squamous cell carcinoma (SCC) were chosen from the Shanxi Tumor Hospital,Second Hospital of Shanxi Medical University,Maternal and Child Health Center in Taiyuan and Jiexiu during September 2009 and March 2011.HPV16 was detected by multiple PCR.FHIT methylation and protein expression levels were detected by methylation specific PCR (MSP) and Western Blot,respectively.All the data were performed with SPSS 20.0 statistical softvare.Differences among groups were assessed by Chi-square and Kruskal-Wallis tests.The interaction effects were evaluated by additive model.Results The prevalence rates of HPV16 infection in CIN1 (45.8％),CIN2+ (68.6％) and SCC (73.0％) were significantly higher than that in NC (28.7％,P＜0.001).In NC,CIN1,CIN2+ and SCC groups,the FHIT gene methylation rates were 3.7％,13.9％,21.4％ and 38.0％ while the protein expression levels were 1.255 ± 0.130,1.184 ± 0.172,1.133 ± 0.126 and 1.099 ± 0.148,respectively.Differences among the groups were statistical significant (P＜0.001).With increasing degrees of cervical lesions,the HPV16 infection rate (x2=47.623,P＜0.001),FHIT methylation rate (x2=40.147,P＜0.001) and the rate of FHIT protein low expression (x2=65.098,P＜0.001) were all gradually increasing.There appeared positive additive interaction between FHIT methylation,FHIT protein low expression and infection of HPV16.Conclusion Hypermethylation of FHIT gene,low expression of FHIT protein and HPVI6 infection could increase the risk of cervical cancer and precancerous lesions.These results suggested that there might be synergistic action between FHIT gene hypermethylation and HPV16 infection in the progression of cervical cancer and the same was true between the low expression of FHIT protein and HPV 16 infection.

Interaction between fragile histidine triad methylation, protein expression and human papillomavirus 16 infection in cervical carcinogenesis / 中华流行病学杂志

Objective To investigate the association between fragile histidine triad (FHIT) gene methylation,abnormal protein expression and HPV16 infection as well as their interactions in cervical carcinogenesis.Methods A total of 108 patients with normal cervical (NC),142 cases of cervical intraepithelial neoplasia (CIN1,n=72;CIN2 +,n=70),and 100 new cases of cervical squamous cell carcinoma (SCC) were chosen from the Shanxi Tumor Hospital,Second Hospital of Shanxi Medical University,Maternal and Child Health Center in Taiyuan and Jiexiu during September 2009 and March 2011.HPV16 was detected by multiple PCR.FHIT methylation and protein expression levels were detected by methylation specific PCR (MSP) and Western Blot,respectively.All the data were performed with SPSS 20.0 statistical softvare.Differences among groups were assessed by Chi-square and Kruskal-Wallis tests.The interaction effects were evaluated by additive model.Results The prevalence rates of HPV16 infection in CIN1 (45.8％),CIN2+ (68.6％) and SCC (73.0％) were significantly higher than that in NC (28.7％,P＜0.001).In NC,CIN1,CIN2+ and SCC groups,the FHIT gene methylation rates were 3.7％,13.9％,21.4％ and 38.0％ while the protein expression levels were 1.255 ± 0.130,1.184 ± 0.172,1.133 ± 0.126 and 1.099 ± 0.148,respectively.Differences among the groups were statistical significant (P＜0.001).With increasing degrees of cervical lesions,the HPV16 infection rate (x2=47.623,P＜0.001),FHIT methylation rate (x2=40.147,P＜0.001) and the rate of FHIT protein low expression (x2=65.098,P＜0.001) were all gradually increasing.There appeared positive additive interaction between FHIT methylation,FHIT protein low expression and infection of HPV16.Conclusion Hypermethylation of FHIT gene,low expression of FHIT protein and HPVI6 infection could increase the risk of cervical cancer and precancerous lesions.These results suggested that there might be synergistic action between FHIT gene hypermethylation and HPV16 infection in the progression of cervical cancer and the same was true between the low expression of FHIT protein and HPV 16 infection.

Expressions of FHIT in patients with endometriosis / 实用医学杂志

Objective To observe the expression of fragile histidine triad (FHIT) protein in the endometriosis and its significance. Methods 28 pairs of samples of endometrium and ectopic endometrium from endometriosis (EMT) patients (EMT group), and 28 endometrial samples from patients only with myoma of uterus (control group)were tested for the expression of FHIT by immunohistochemical SP method. Results FHIT was mainly expressed in the cytoplasm and membraneof endometrial glandular epithelial cells. The positive rate of FHIT expression in endometriumand ectopic endometrium from intrauterine membrane endometriosis (EMT group) patientwas 68% and 54%, which had no significant difference (P > 0.05). However, the positive rate of FHIT expression in control group was 96% (27/28), which is higher than those in the EM group, and the differences were statistically significant. The expression of FHIT was different indifferent stages of r-AFS in ectopic endometrium samples. The expression in stage Ⅰ-Ⅱ is higher than in stage Ⅲ-Ⅳ, with statistical significance. Conclusions FHIT may have some correlation with the development of endometriosis , and may have some influence on the severity of this disease.

Loss of fragile histidine triad gene expression in papillary thyroid carcinoma / 中华内分泌外科杂志

Objective To study fragile histidine triad gene(FHIT) gene mRNA expression in 60 samples of papillary thyroid carcinoma(PTC) and matched adjacent non-concerous tissues (NCE),and to explore the role of FHIT gene in the development in PTC.Methods Reverse transcription polymerase chain reaction(RT-PCR) was used to detect FHIT gene mRNA expression in 60 samples of PTC and matched NCE.Results In PTC tissues,the positive rate of FHIT gene mRNA expression was 45.0％ (27/60),lower than that in NCE tissues (100.0％,60/60).FHIT gene mRNA expression was correlated with pathology stage,TNM stage and lymph node metastasis (P ＜ 0.05).Conclusion FHIT loss and transcript abnormality might play important roles in proliferation and metastasis of PTC,and might be a useful marker for evaluating the biological behavior of PTC.

Influence of folate on fragile histidine triad gene expression,cell proliferation and apoptosis in cervical cancer cell lines / 中华流行病学杂志

Objective To explore the effect of folate on cell proliferation and apoptosis as well as on DNA methylation,expression of mRNA and protein of fragile histidine triad(FHIT)gene in cervical cancer cells. Methods Cervical cancer cell lines including CaSki(HPV16-positive)and C33A(HPV-negative)were cultured in vitro with different folate concentrations. Cell proliferation and apoptosis were determined by viable cell counting and flow cytometry while FHIT gene DNA methylation was used with methylation specific PCR(MSP). Both gene expression of FHIT protein and mRNA were detected by Western blot and Real-time PCR,respectively. Results Folate could inhibit the proliferation and promote the apoptosis in two kinds of cervical cancer cells. The number of viable cells decreased (C33A:r=0.98,P<0.001;CaSki:r=0.98,P<0.001) and the apoptosis rate increased(C33A:r=0.98,P<0.001;CaSki:r=0.99,P<0.001)along with the increase of folate concentration. FHIT gene DNA methylation showed all positive at the folate concentration levels of 1μg/ml and 10μg/ml,partially positive at 100μg/ml and 250μg/ml,but negative at 500μg/ml and 1 000μg/ml in both C33A and CaSki cells. Comparing with the control group,the mRNA or protein relative expression levels of FHIT gene in different folate concentrations were statistically significant in two kinds of cells,and showing that the FHIT gene mRNA expression(C33A:r=0.96,P<0.001;CaSki:r=0.94,P<0.001)and protein expression (C33A:r=0.96,P<0.001;CaSki:r=0.97,P<0.001) both increased along with the increase of folate concentration. Conclusion Our findings indicated that adequate folate seemed to be able to effectively inhibit the proliferation of cervical cancer cells and facilitate their apoptosis in vitro,so would reverse the aberration mRNA and protein expression of FHIT gene.

Influence of folate on fragile histidine triad gene expression,cell proliferation and apoptosis in cervical cancer cell lines / 中华流行病学杂志

Objective To explore the effect of folate on cell proliferation and apoptosis as well as on DNA methylation,expression of mRNA and protein of fragile histidine triad(FHIT)gene in cervical cancer cells. Methods Cervical cancer cell lines including CaSki(HPV16-positive)and C33A(HPV-negative)were cultured in vitro with different folate concentrations. Cell proliferation and apoptosis were determined by viable cell counting and flow cytometry while FHIT gene DNA methylation was used with methylation specific PCR(MSP). Both gene expression of FHIT protein and mRNA were detected by Western blot and Real-time PCR,respectively. Results Folate could inhibit the proliferation and promote the apoptosis in two kinds of cervical cancer cells. The number of viable cells decreased (C33A:r=0.98,P<0.001;CaSki:r=0.98,P<0.001) and the apoptosis rate increased(C33A:r=0.98,P<0.001;CaSki:r=0.99,P<0.001)along with the increase of folate concentration. FHIT gene DNA methylation showed all positive at the folate concentration levels of 1μg/ml and 10μg/ml,partially positive at 100μg/ml and 250μg/ml,but negative at 500μg/ml and 1 000μg/ml in both C33A and CaSki cells. Comparing with the control group,the mRNA or protein relative expression levels of FHIT gene in different folate concentrations were statistically significant in two kinds of cells,and showing that the FHIT gene mRNA expression(C33A:r=0.96,P<0.001;CaSki:r=0.94,P<0.001)and protein expression (C33A:r=0.96,P<0.001;CaSki:r=0.97,P<0.001) both increased along with the increase of folate concentration. Conclusion Our findings indicated that adequate folate seemed to be able to effectively inhibit the proliferation of cervical cancer cells and facilitate their apoptosis in vitro,so would reverse the aberration mRNA and protein expression of FHIT gene.

FHIT gene and tumor / 国际肿瘤学杂志

The human fragile histidine triad (FHIT) gene is a tumor suppressor gene,which is located at chromosome region 3p14.2.The fragile site FRA3B of the FHIT gene is the most unstable site.FHIT can promote apoptosis,and inhibit cell proliferation and tumorigenesis.High methylation status,loss of the various sections of the FHIT gene,changes of the fragile site FRA3B and abnormalities of FHIT transcripts can result in gene afunction,and then promote the development and progression of various types of cancers.Transfecting wild-type FHIT into tumor cells with low or lacking endogenous FHIT expression can induce apoptosis.The combined treatment with other genes may provide a new insight for the treatment of tumors.

Effects of exogenous fragile histidine triad gene on apoptosis of MGC-803 gastric cancer cells induced by octreotide / 肿瘤

Objective:To investigate the effect of exogenous extopic fragile hisdidine triad (FHIT) gene on the apoptosis of gastric cancer cells induced by octreotide and elucidate the underlying mechanism. Methods: Human gastric cancer cell line MGC-803, which was loss of FHIT gene, was transfected with plasmid pRcCMV-FHIT and pRcCMV via lipofectamine mediation. After transfection, Western blotting was used to analyse the expression of FHIT protein in positive cells screened out by G418. The cells were treated with octreotide 10~(-10), 10~(-9), 10~(-8), 10-7, and 10~(-6) mol/L for 24, 48 and 72 h. Cell proliferation was evaluated by MTT assay and apoptosis by flow cytometry. The expression of bcl-2 and bax protein was detected with Western blotting.Results:FHIT protein expression was detected in MGC-803 gastric cancer cells after FHIT gene transfection. After treatment with octreotide 10~(-8) mol/L for 48 h, the apoptotic rate of MGC-803 cells transfected with FHIT gene was (26.777±1.702)%, significantly higher than that in empty vector group and untransfected group [(13.800±0.511)% vs (12.634±0.479)%, F=245.789, P<0.05]. The expression of bcl-2 protein was decreased while the expression of bax protein was increased in FHIT gene transfection group after octreotide treatment. Conclusion:The exogenous FHIT gene and octreotide had strong synergistic effects on apoptosis of MGC-803 cell lines, and their action mechanism may be related to the alteration of the expression of apoptosis-related proteins of bcl-2 family.

Expression of Livin protein and its relationship with Caspase-3, FHIT protion in skin squamous cell carcinoma / 肿瘤研究与临床

Objective To study the expression of Livin and its relationship with Caspase-3, FHIT in skin squamous cell carcinoma. Methods lmmunohistochemical assay was used to detect the expression of Livin, Caspase-3 and FHIT in 48 cases of sSCC, 20 cases of chronic ulcer and 12 cases of normal skin tissues. Results The rate of positive expression of Livin in SCC tissues was significantly higher than that in the chronic ulcer tissues and normal skin tissues (P <0.01). The rate of positive expression of Caspase-3 and FHIT in SCC tissues was significantly lower than that in the chronic ulcer tissues and normal skin tissues (P < 0.01).The expression of Livin and Caspase-3 had relationship with the lymphatic metastasis and histologic differentiation of SCC(P <0.05). The expression of Livin and Caspase-3 had not relationship with age, sex, the sizes of SCC (P >0.05). There was negative significant correlation between the expression of Livin and the expression of Caspase-3, FHIT. Conclusion There may be relationship between the abnormal expression of Livin and Caspase-3, FHIT and the occurrence, progression of skin squamous cell carcinomas. They may become a new method for preservation and treatment skin of squamous cell carcinomas.

The aberrant methylation of fragile histidine triad (FHIT) gene and its significance of the expression of FHIT protein in lung cancer / 肿瘤

Objective: To detect the expression of fragile histidine triad (FHIT) protein and aberrant methylation of its gene in lung carcinoma tissue and discuss their significance in tumorigenesis of lung cancer. Methods: The expression of FHIT protein was determined by immunohistochemical SP staining and its aberrant methylation was detected by methylation-specific PCR (MSP) in lung cancer and adjacent lung tissues (n = 60). The sequencing of the amplified products of MSP was performed. The 60 patients were followed up. Results: The expression of FHIT protein in adjacent lung tissues was obviously higher than that in lung cancer tissues. There was significant difference between them (76.7% vs 50%, P 0.05). The survival time was longer in FHIT-positive patients than FHIT-negative patients (P <0.05). The FHIT protein was the risk factor associated with the disease-free survival time of patients (P <0.01). Conclusion: The aberrant methylation of FHIT gene occurrs frequently and the expression of FHIT protein is significantly down-regulated in lung cancer. FHIT may play an important role in the tumorigenesis and development of lung cancer. FHIT protein could be used as an important factor for predicting the prognosis of patients.

Research on tumor suppressor gene FHIT / 上海第二医科大学学报

Fragile histidine triad(FHIT) gene is a tumor suppressor gene that locates on chromosome 3p14.2.FHIT can induce cell apoptosis and inhibit cell growth by activating caspase,inhibiting PI3K-Akt-survivin signal pathway and phosphorylation of I?B-?,and binding with microtube.The inactivation of FHIT is closely related with carcinogenesis.The advances in research on the structure,biological function,relationship between inactivation and carcinogenesis,and gene therapy of FHIT are reviewed in this paper.

Effects of exogenous FHIT gene on proliferation and apoptosis of human glioma cell line U87 / 上海第二医科大学学报

Objective To investigate the effects of exogenous fragile histidine triad(FHIT) gene on apoptosis of human glioma cell line U87. Methods By the method of liposome transfection,plasmids pcDNA3.1/myc-His(-)B-FHIT and pcDNA3.1/myc-His(-)B were transfected into glioma cell line U87.U87 cells were divided into three groups: U87-FHIT group,U87 cells transfected by plasmids pcDNA3.1/myc-His(-)B-FHIT;U87-vector group,U87 cells transfected by plasmids pcDNA3.1/myc-His(-)B;and blank control group,U87 cells without transfection.The expression of exogenous FHIT protein was detected by Western blot and immunofluorescence staining.The effects of FHIT on the growth characteristics of U87 were observed by MTT and flow cytometry. Results Growth inhibitory rate and apoptosis rate of the cells in U87-FHIT group were significantly higher than those in U87-vector group and blank control group(P

Effect of the exogenous fragile histidine triad(FHIT)gene on the proliferation and apoptosis of cutaneous carcinoma cell line A431 / 基础医学与临床

Objective To investigate the effect of the exogenous fragile hisdidine triad(FHIT) gene on the proliferation and the apoptosis of cutaneous carcinoma cell line A431,and to explore the mechanism of tumor suppression by the FHIT gene.Methods The plasmids pcDNA3-FHIT and pcDNA3-vector were transfected into the cutaneous carcinoma cell line A431 without FHIT gene expression,and then the transfected cells were screened by G418 and the expression of FHIT was determined by the immunocytochemical staining technique.The effect of FHIT on the growth characteristics of cutaneous carcinoma cell line A431 was observed by MTT,colony forming test and flow cytometry.Results Stable FHIT gene expressing A431 cells were produced,the proliferation activity and colony forming capability of A431FHIT were suppressed,whereas the apoptosis was increased.All these differences between A431-FHIT cells and the two control groups of cutaneous carcinoma cells had statistical significance.Conclusion Transfecting the exogenous FHIT gene into cutaneous carcinoma cells line A431can suppress the proliferation of tumor cells,and can also induce apoptosis and cell cycle arrest.

Expression of FHIT in oral squamous cell carcinoma and significance / 吉林大学学报(医学版)

Objective To study the expression of fragile histidine triad(FHIT) in oral squamous cell carcinoma(OSCC),and discuss its role and significance in OSCC.Methods Immunohistochemical method was used to detect the expressions of FHIT in 48 cases of OSCC and 26 normal oral mucosa.Results The positive expression rate of FHIT in normal oral mucosa was 76.92%(20/26).Among 48 OSCC patients,the positive rate of FHIT(43.75%) was lower than that in normal oral mucosa(P0.05),but FHIT protein content was significantly associated with differentiation(P

Expressions of FHIT in cervical cancer and cervical intraepithelial neoplasia / 吉林大学学报(医学版)

Objective To study the expressions of fragile histidine triad(FHIT) in cervical cancer and cervical intraepithelial neoplasia(CIN),and the relationship between the FHIT expression and the tumor occurance and development in cervical cancer.Methods The expressions of FHIT in cervical cancer tissue of 35 patients,39 CIN samples and 16 normal cervix tissue were detected by SP immunohistochemical method and the relations with occurance,pathologic type,histological grade,clinical pathologic staging and lymph node metastasis in cervical cancer were analyzed.Results FHIT expressed in normal cervical tissue,CIN and cervical cancer tissue,which showed a decreasing trend(P0.05).(Conclusion Expression)of FHIT has close relations with the tumor occurance and development in cervical cancer,which could provide a reference foundation to monitor lapse of CIN and judge prognosis of cervical cancer.

Expression of fragile histidine triad gene in endometrial carcinoma and its significance / 吉林大学学报(医学版)

0.05).Conclusion The reduced expression of FHIT may be associated with endometrium canceration and may be not associated with surgical pathologic staging,lymph node metastatic and depth of myometrial invasion in endometrial carcinoma.The reduced expression of FHIT indicates the pathogenesis of endometrial carcinoma.

Effect of Trichostatin A on Apoptosis of Human Hepatoma Cell Line HepG2 and Expression of FHIT and Apoptosis-related Proteins / 中国药房

OBJECTIVE: To investigate the effect of trichostatin A (TSA),a specific inhibitor of histone acetyltransferase,on apoptosis of human hepotoma cell line HepG2,the expression of fragile histidine triad (FHIT) and apoptosis-related proteins in order to study apoptosis mechanisms.METHODS: Human hepatoma cell lines HepG2 were cultured and treated with different concentrations of TSA(125,250,500,1 000,2 000 nmol?L-1) for 24 and 48 hours.Human hepatoma cell lines HepG2 survival and apoptosis were determined by MTT assay with absorbance vale and inhibitory rate as index.Apoptotic percentage of HepG2 treated with 250 and 1 000 nmol?L-1 TSA were determined using TUNEL assay.The expressions of FHIT and caspase-3,bax,bcl-2 were analyzed by immunocytochemistry with solvent as control.RESULTS: As compared with control group,absorbance vale of human hepatoma cell lines HepG2 were decreased after treated with different concentration of TSA in dose-dependent and time-dependent manners.Positive cell rate in TUNEL was increased (P0.05).CONCLUSION: TSA may inhibit proliferation and promote apoptosis of hepatoma HepG2 cell by up-regulating the protein expression of FHIT,caspase-3 and bax.