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Purpose To clarify the role of KAI1/CD82 in metastasis of nasopharyngeal carcinom and to evaluate the clinical efficacy of KAI1/CD82-expressing EPCs in the prevention of nasopharyngeal carcinoma.Method Umbilical vein-derived EPCs were infected with KAI1/CD82-expressing lenti-virus to get a KAI1/CD82-overexpressing EPC cell line (KAI1/CD82-EPCs).A xenograft mouse model of human nasopharyngeal carcinoma was established,and KAI1/CD82-EPCs were injected through the tail vein.The effect of the KAI1/CD82-EPCs on growth and metastasis of the xenograft was observed.Results Time required for tumor formation was 14.70 ± 3.81,15.05 ±3.85,14.20 ± 3.55 days respectively for the EPCs,EPCs-NC,and KAI1/CD82-EPCs groups,with no significant difference among the three groups (P =0.771).Weight of the xenograft was (1.388 ±0.204) g,(1.487 ±0.223) g,(1.485 ±0.234) g respectively for the EPCs,EPCs-NC,and KAI1/CD82-EPCs groups,with no significant difference (P =0.274).Rate of lung metastasis was 55％,45％ and 10％ for the EPCs,EPCs-NC,and KAI1/CD82-EPC groups,and the difference was significant (P =0.005).Number of metastatic lesions was 34.27 ± 5.35,38.44 ± 9.63,17.50 ± 3.54 for the three groups,and the difference was also significant (P =0.007).Immunohistochemistry indicated positive KAI1/CD82 expression in metastatic lesion of the KAI1/CD82-EPCs group,but no KAI1/CD82 expression in the EPCs group or EPCs-NC group.Conclusion KAI1/CD82-expressing EPCs inhibits lung metastasis of the xenograft mouse model of human nasopharyngeal carcinoma.
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Objective: To evaluate the effect of imatinib mesylate on cell viability, anti cancer effect through modulation of KAI1/CD82 gene expression in breast cancer MCF-7 cell line. Methods: The effects of imatinib mesylate on cell viability in MCF-7 cell line were assessed using MTT assay and IC
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Purpose To study the expression of metastasis suppressor gene (KAI1/CD82) and cell adhesion molecules(CD44v6) in human laryngeal squamous cell carcinoma ( LSCC) and its clinical significance, and to investigate their relationship. Methods EnVi-sion immunohistochemistry was used to detect the expression of KAI1/CD82 and CD44v6 protein in 64 cases of LSCC tissues and 15 ca-ses of normal laryngeal mucosa ( NLM) tissues. Results The positive rate of KAI1/CD82 in LSCC tissues ( 37. 50%) was signifi-cantly lower than that of the NLM tissues(86. 67%) (P=0. 031), and the positive rate of CD44v6 in LSCC tissues(75. 00%) was significantly higher than that of the NLM tissues(26. 67%) (P=0. 011). The expression of KAI1/CD82 was associated with clinical stages, grade of tumor differentiation, neck lymph node metastasis ( P0. 05). And CD44v6 with grade of tumor differentiation, neck lymph node metastasis and prognosis (P0. 05). In addition, KAI1/CD82 expression was negatively correlated with CD44v6 expression (rs = -0. 504, P=0. 036). Conclusion KAI1/CD82 and CD44v6 are mutually inhibited in the tumorigenesis, progress, invasion and metastasis, and detection of the expression of KAI1/CD82 and CD44v6 may be helpful for judging the biological behaviors of LSCC.
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Objective To study the expression of metastasic suppressor gene( KAI1 / CD82)and cell adhesion molecules(CD44v6)in human laryngeal squamous cell carcinoma(LSCC),precancerous lesion,polyps,and normal mucosa. Methods Immunohistochemical technique( Envision)was used to detect the expression of KAI1 / CD82 protein and CD44v6 protein in 64 cases of LSCC,21 cases of laryngeal precancerous lesion(LPL),15 cases of polyp of larynx(LP)and 15 cases of normal laryngeal mucosa(NLM). Results The result turned out to be as follows:①KAI1 / CD82 protein was highly expressed in NLM and LP,and lowly expressed in LPL and LSCC,the positive rates of KAI1 / CD82 protein expression were 86. 67%(13 / 15),80. 00%(12 / 15),38. 10%(8 / 21)and 37. 50%(24 /64),respectively. There was statistically significant difference in NLM and LSCC. ② CD44v6 protein was lowly ex-pressed in NLM and LP and highly expressed in LPL and LSCC,the positive rates of CD44v6 protein expression were 26. 67%(4 / 15),33. 33%(5 / 15),80. 95%(17 / 21)and 75. 00%(48 / 64),respectively. There was statisti-cally significant difference in NLM and LSCC. Conclusion ① The down-regulation or deletion of KAI1 / CD82 and the up-regulation of CD44v6 are related to carcinogenesis,development of LSCC. ② The combined detection of KAI1 / CD82 and CD44v6 may provide clinical basis for the early diagnosis of LSCC.
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BACKGROUND: Patients with diabetes mellitus often have a difficult life, suffering from foot ulceration or amputation. Diabetes is characterized by chronic inflammation, and one of the features of inflammation is hypoxia. Recently, it has been reported that KAI1 is a hypoxia target gene. There is no published research on hypoxia-related KAI1 protein levels in human diabetic skin. Therefore, we have investigated the expression of KAI1 protein in diabetic skin tissue in vivo. METHODS: The expression of KAI1 protein was evaluated by western blotting in 6 diabetic skin tissue samples and 6 normal skin samples. Immunohistochemical staining was carried out to identify KAI1 expression. RESULTS: The western blotting revealed significantly increased expression of the KAI1 protein in diabetic skin tissues as compared to normal skin tissues. Immunohistochemical examination demonstrated that KAI1 was expressed in all diabetic skin tissues with moderate-to-strong positivity and weakly expressed in normal skin tissues. CONCLUSIONS: Our data suggest that a high expression of the KAI1 protein can be observed in diabetic skin tissue. To the best of our knowledge, this is the first report suggesting that KAI1 protein expression in diabetic skin tissues may be associated with chronic inflammatory states and hypoxia.
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Humans , Amputation, Surgical , Hypoxia , Kangai-1 Protein , Blotting, Western , Diabetes Mellitus , Foot Ulcer , Inflammation , SkinABSTRACT
Objective Uterine epithelial cells were isolated from pregnant mice and cultured in vitro , and exam-ined the effect of CD82 on the expression of integrin αV,β3, E-cadherin and β-catenin in the cells.Methods The uter-ine epithelial cells were primarily isolated from pregnant mouse uterus .The recombinant adenovirus containing mouse CD 82 gene which had been constructed in our lab infected the uterine epithelial cells .Immunocytochemistry was used to detect the protein expressions of integrin αV,β3, E-cadherin and β-catenin in the uterine epithelial cells , which were infected with CD82 adenovirus or not .Results 1.The purity of primary cultured cells was (93.2 ±0.6)%.2.The transfection efficiency of CD82 recombinant adenovirus was ( 92 ±4.5 )%.The adenoviral particles carrying CD 82 gene indeed ex-pressed CD82 gene and protein in the primary uterine epithelial cells after 24 hours or 48 hours.3.The uterine epithelial cells of pregnant mice on d4 expressed integrin αV, β3, E-cadherin and β-catenin.4.In contrast to the control group, when CD82 adenovirus infected cells , the uterine epithelial cells of pregnant mice on d 4 increased the expression of integrinαV,β3 and β-catenin protein, had no significant changes of E-cadherin.Conclusions CD82 may have effect on the ex-pression of integrin αV,β3 and β-catenin in mouse uterine epithelial cells before implantation .
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Acute myeloid leukemia with maturation (AML-M2) is associated with the 8;21 translocation. For the first time in an adult patient with AML-M2, a novel unbalanced translocation involving the short arm of chromosome 11 and long arm of chromosome18 with new breakpoints is presented. CD82 on band 11p11.2 and GATA 6 on 18q11.2 may play a role in the pathogenesis of de novo AML M2. The report with translocation (11;18)(p11.2;q11.2), as the sole cytogenetic abnormality provides more data on the leukemogenesis of de novo AML M2.
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Objective To explore the expression of KAI1/CD82,E-cadherin and β-catenin in endometrial carcinoma,and to investigate their correlations to clinicopathological parameters of endometrial carcinoma. Methods The expressions of KAI1/CD82,E-cadherin and β-catenin in 76 specimens of endometrial carcinoma,15 specimens of atypical endometrial hyperplasia and 20 specimens of proliferative endometrium were examined by immunohistochemical envision technique.Their correlations to clinicopathological parameters of endometrial carcinoma were statistically analyzed. Results Compare to normal proliferative phase endometrium and atypical endometrial hyperplasia,the expression of KAI1/CD82 in endometrial carcinoma was significantly decreased(P ＜0.01),the abnormal expression of E-cadherin and β-catenin in endometrial carcinoma were significantly higher(all P <0.01).In endometrial carcinoma,the expression of KAI1/CD82 was negative correlated with histological grade and depth of myometrial invasion(P <0.01,P <0.05); The abnormal expression of the E-cadherin is related to histological grade and type(P <0.01,P<0.05); The abnormal expression of β-catenin was positively correlated with histological grade and FIGO stage(P ＜0.01 ,P <0.05).The down-regulation expression of KAI1/CD82 was closely associated with the abnormal expression of E-cadherin and beta-catenin in endometrial carcinoma(P <0.01,P <0.05). Conclusion The down-regulation of KAI1/CD82 and the aberrant expression of E-cadherin and β-catenin could be involved in the development of endometrial carcinoma.The loss or reduced expression of KAI1/CD82 was closely associated with the abnormal expression of E-cadherin and β-catenin in endometrial carcinoma.
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Objective: To study the effect of metastasis suppressor gene Kail/CD82 on the cell proliferation of Hep-2 cell line. Methods: Recombinant adenovirus rAd-Kail was amplified, purified, and was used to transfect laryngo-carcinoma Hep-2 cell line. Cells transfected with blank vector and untransfected cells served as controls. MTT assay was used to assess the influence of Kail gene on proliferation of Hep-2 cells; RT-PCR was used to examine the expression of Kail gene in cells of different groups. Results: The titer of rAd-Kail reached 6 X 1010 PFU/ml after expansion and purification. When the concentration of the adenovirus was 30 MOI, the transfection rate of Hep-2 cells could be higher than 90%. MTT assay showed that the cell proliferation abilities were similar in the two control groups, and the proliferation ability of cells in the Kail transfection group was significantly lower than that in the non-transfected group (P<0. 05) ,with the inhibitory rate in the Kail group being 29%. Conclusion: The Kail/CD82 gene can inhibit the proliferation of Hep-2 cells.
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Objective To explore the effects of hypoxia (1% O2) on the ability of cell invasiveness and expression of KAI1/CD82 in SMMC7721 hepatocellular carcinoma cells. Methods SMMC7721 hepatocellular carcinoma cells were cultured by hypoxia ( 1% O2) in vitro, and the ability of cell invasiveness was analyzed by cell invasion assay.Immunohistochemistry staining technique was used to evaluate the protein expression of KAI1/CD82. Results Cell invasion assay revealed that hypoxia enhanced the ability of invasiveness of hepatocellular carcinoma cells. In addition,KAI1/CD82 protein expression was positive in cultured SMMC7721 hepatocellular carcinoma cells, and it was located diffusedly in the cytoplasm and on the membrane. KAI1/CD82 protein expression was down-regulated when mediated by hypoxia; at the same time, it showed a time-effect relationship. Conclusion Hypoxia can enhance invasiveness of hepatocellular carcinoma cells. The down-regulation of KAI1/CD82 expression may play a certain role in those courses.
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Objective: To explore the effects of hypoxia (1% O2) on the ability of cell invasiveness and expression of KAI1/CD82 in SMMC7721 hepatocellular carcinoma cells. Methods: SMMC7721 hepatocellular carcinoma cells were cultured by hypoxia (1% O2) in vitro, and the ability of cell invasiveness was analyzed by cell invasion assay. Immunohistochemistry staining technique was used to evaluate the protein expression of KAI1/CD82. Results: Cell invasion assay revealed that hypoxia enhanced the ability of invasiveness of hepatocellular carcinoma cells. In addition, KAI1/CD82 protein expression was positive in cultured SMMC7721 hepatocellular carcinoma cells, and it was located diffusedly in the cytoplasm and on the membrane. KAI1/CD82 protein expression was down-regulated when mediated by hypoxia; at the same time, it showed a time-effect relationship. Conclusion: Hypoxia can enhance invasiveness of hepatocellular carcinoma cells. The down-regulation of KAI1/CD82 expression may play a certain role in those courses.
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Objective To investigate the correlation of the expression of KAI1/CD82 and laminin receptor (LNR) in cholangiocarcinoma, and study its role in the invasion and metastasis of cholangiocarcinoma. Methods The expressions of KAI1/CD82 and LNR in 48 cholangiocarcinoma tissue samples were detected by SP immunohistochemistry, and their relationships with clinicopathological factors were analyzed. Results The positive expression rates of KAI1/CD82 and LNR in cholangiocarcinoma were 31% (15/48) and 54% (26/48), respectively. In highly differentiated cholangiocarcinoma, the positive expression rate of KAI1/CD82 was high (χ2=3.911, P<0.05), while that of the LNR was low (χ2=6.970, P<0.05). The positive expression rate of KAI1/CD82 in cholangiocarcinoma with metastasis was significantly lower than that in cholangiocarcinoma without metastasis (χ2=5.765, P<0.05), while the positive expression rate of LNR in cholangiocarcinoma with metastasis was significantly higher than that in cholangiocarcinoma without metastasis (χ2= 9.952, P<0.05). The expression level of KAI1/CD82 was negatively correlated with that of the LNR ( r = -0.462, P < 0.01 ). Conclusions The up-regulated expression of LNR in cholangiocarcinoma correlates with the decreased expression of KAI1/CD82, and plays an important role in the invasion and metastasis of cholangio-carcinoma.
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The expression of KAI1/CD82 and MRP-1/CD9 in transitional cell carcinoma of bladder (TCCB) and its clinical significance were investigated. Immunohistochemistry was used to detect KAI1/CD82 and MRP-1/CD9 protein expression in 52 TCCB specimens. Correlation between the expression of KAI1/CD82 and MRP-1/CD9 to clinicopathologic factors was statistically analyzed. The results showed that the positive rate of KAI1/CD82 and MRP-1/CD9 in TCCB was 50% and 61.5%, respectively. The MRP-1/CD9 and KAI1/CD82 expression was significantly associated with grade of TCCB (P＜0.05), but no correlation was found between MRP-1/CD9 or KAI1/CD82 expression and clinical stage of TCCB (P＞0.05). The expression level of MRP-1/CD9 and KAI1/CD82 in recurrent TCCB samples was lower than that in non-recurrent samples (P＜0.05). Meanwhile, the correlation between the KAI1/CD82 expression and MRP-1/CD9 expression was statistically significant (r=0.316, P＜0.05). It was concluded that KAI1/CD82 and MRP-1/CD9 expression may be important prognostic indicators and potentially useful for assessing the biological behavior of TCCB.
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Objective To investigate the effect of recombinant adenovirus containing CD82/KAI1 on the expressions of integrin ?5,integrin ?3,MMP-9,E-cadherin and ?-catenin in uterine stromal cells.Methods Uterine stromal cells were isolated from pregnant mice during implantation window and cultured primarily.The recombinant adenovirus containing mouse CD82/KAI1 gene was constructed.Protein expression of integrin ?5,integrin ?3,MMP-9,E-cadherin and ?-catenin were detected by immunocytochemical methods in the cultured cells with or without CD82/KAI1 adenovirus transfection.Results When the cells which were cultured for 48 h were transfected with the recombinant adenovirus vector at a titer of 6.5?1012 pfu/ml,CD82/KAI1 were obviously upregulated in the primary uterine stromal cells.In the uterine stromal cells from pregnant mice on the 4 d after gestation,integrin ?5,E-cadherin,?-catenin and MMP-9 were detected,while,integrin ?3 were not.But in the cells of nonpregant rats,no expression of these 5 proteins was found.Compared with the cells transfected with blank adenovirus,the recombinant adenovirus encoding CD82/KAI1 upregulated the expressions of ?-catenin and MMP-9(P0.05)and no integrin ?3 was detected in the stromal cells of pregnant mice on day 4 of gestation.Conclusion The recombinant adenovirus containing mouse CD82/KAI1 gene is successfully constructed.CD82/KAI1 might have certain effect on the expressions of integrin ?5,MMP-9,E-cadherin and ?-catenin in mouse uterine stromal cells before embryo implantation.
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Objective To study the expression of KAI1/CD82 in non-small cell lung carcinomas(NSCLC) and explore the mechanism of invasion and metastasis of tumor cells.Methods The S-P immunohistochemistry was used to detect the expression of KAI1/CD82 in 62 specimens of primary NSCLC and 22 specimens of lymph node metastatic tissues. Twenty specimens from the normal tissues adjacent to the tumor over 5 cm were used as negative controls.Results The expression level of KAI1/CD82 in NSCLC(32.26%) was lower than that in negative control tissues(85.0%) (P
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Although reduced expression of CD82 transmembrane protein facilitates metastasis of cancer cells, little is known about its biological function. Here we have investigated the role of CD82 in B cell lymphocyte adhesion. When IM-9 cells were engaged with anti-CD82 monoclonal antibody, they formed homotypic aggregates in a short time. This adhesion was inhibited by anti-CD11a monoclonal antibody that has been known to block LFA-1-mediated cell adhesion. The cell surface expression of LFA-1 has not been changed by CD82 engagement. Homotypic aggregation was decreased in the cells in which the level of CD82 expression was low, and it was not recovered by anti-CD99 monoclonal antibody or PMA that has been known to stimulate cell adhesion. In addition, it was recovered by Mg++ treatment that induces conformational change of LFA-1 moleucles, but not by Ca++ treatment that leads to clustering of LFA-1 on the cell surface. CD82-induced cell aggregation was dramatically abrogated by addition of the phos-phatidylinositol 3-kinase (PI3-K) inhibitor LY294002 or p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580. Taken together, these results suggest that CD82 molecule may fascilitate adhesion of lymphocytes by inducing conformational change of LFA-1 to pro-adhesive structure through PI3-K or p38 MAPK signal pathway.
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Cell Adhesion , Cell Aggregation , Cell Line , Lymphocyte Function-Associated Antigen-1 , Lymphocytes , Neoplasm Metastasis , p38 Mitogen-Activated Protein Kinases , Protein Kinases , Signal TransductionABSTRACT
Objective To investigate the expression and significance of KAI1/CD82 and E-Cadherin in human squamous cervical carcinoma.Methods The expressions of KAI1/CD82 and E-Cadherin were examined respectively by immunohistochemical S-P method in 10 cases of normal cervical tissue,15 cases of atypical hyperplasia of cervical epithelia and 64 cases of squamous cervical carcinoma.We analyzed statistically the correlation between the immunohistochemical results and the clinicopathological features.Results From normal cervical tissue,Cervical intraepithelial neoplasis(CIN) to cervical cancer,the positive expression rates of KAI1/CD82 and E-Cadherin were gradually decreased.Through statistic test,the positive expression rates of both invasive squamous carcinoma of the cervix were significantly lower in normal cervical tissue and CIN(P0.05).Of all the samples,direct correlation was showed in the expressions of KAI1/CD82 and E-Cadherin.Furthermore,the low-expression of both revealed significant correlation with lymphonode metastasis in human squamous cervical carcinoma.Conclusion KAI1/CD82 and(E-Cadherin) interactions may depress lymphonode metastasis in cervical carcinoma.Logistic analysis reveals that(E-Cadherin) gene,specific and interactions of several genes may be more significant during tumor metastasis.