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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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Objective To observe the inhibitory effect on lymph node metastasis of pancreatic cancer and lymphangiogenesis in mice by injection of KAll gene within xenograft tumor.Methods Pancreatic cancer cell line MiaPaCa-2 wag used to construct the nude mice models bearing tumors,then the mice were divided into normal saline group,Ad group and Ad-KAI1 group.Since the successful model construction,normal saline,Ad,Ad-KAI1 was injected every week for 3 times,respectively in the three groups,then the tumor size was documented.50 d after model construction,the tumor and enlarged lymph nodes were collected and subjected to pathological exam,and the expression of LYVE-1 and the MLVD in xenograft tumor was detected by immunohistochemistry.Results Two weeks after MiaPaCa-2 implantation,the model was 100％ successfully constructed.The growth curve of subcutaneous tumor among 3 groups was not statistically significant (P＞0.05) ; the weights of subcutaneous tumor in the 3 groups were (2514.4 ±351.3),(2466.1 ± 295.5),(2294.4±255.4) mg after 50 d,and the difference among the 3 groups was not statistically significant (P ＞0.05).Enlarged lymph nodes metastasis was observed in 8 mice (80％) in normal saline group,and 20 lymph nodes were collected,with 2.0 lymph nodes per mice; and enlarged lymph nodes metastasis was observed in 7 mice (70％) in Ad group,and 15 lymph nodes were collected,with 1.5 lymph nodes per mice; while enlarged lymph nodes metastasis was observed in 4 mice (40％) in Ad-KAI1 group,and 6 lymph nodes were collected,with 0.6 lymph nodes per mice.All the lymph nodes were confirmed to be metastasis of the primary tumor after pathologic exam.The difference of lymph nodes metastasis,number of lymph nodes metastasis per mice among the 3 groups was statistically significant (F =3.14,3.35,P ＜ 0.05).The MLVD of subcutaneous tumor among the 3 groups was (18.70 ± 5.60),(19.40 ± 4.58),(9.80 ±4.10)/400 times magnification,the MLVD of Ad-KAI1 group was significantly lower than those in normal saline group and Ad group (F10.76,11.36,P ＜ 0.05),but the difference between normal saline group and Ad group was not statistically significant.Conclusions KAI1 can inhibit the lymph node metastasis of pancreatic cancer,and the mechanism may be related with decreased lymphangiogenesis and reduced lymphatic vessel density.
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BACKGROUND/AIMS: We tried to investigate the expression characteristics of KAI1, a suppressor of wide-spectrum tumor metastasis, and vascular endothelial growth factor (VEGF), the most common angiogenesis factor, and then to analyze their diagnostic value for hepatocellular carcinoma (HCC). METHODS: The protein and mRNA expression levels of KAI1 or VEGF in HCC tissues and in self-controlled para-carcinoma tissues were analyzed by Western blot and real-time polymerase chain reaction, respectively. Serum levels of KAI1 and VEGF in the patients with HCC, benign liver disease or in healthy controls were quantitatively detected by enzyme-linked immunosorbent assay. RESULTS: The expression level of KAI1 was downregulated, while the expression level of VEGF was upregulated in the tissues or serum of the patients with HCC. The expression level of serum KAI1 in HCC patients was correlated with TNM staging, intrahepatic metastasis, lymph node or peritoneal metastasis, and portal vein thrombus. In addition to the factors that were correlated with KAI1 expression, VEGF expression was also closely related to the alpha-fetoprotein level of the patients. The area under the receiver operating characteristic curve for the diagnosis of HCC was 0.907 for KAI1 and 0.779 for VEGF. The sensitivity of serum KAI1 levels in the diagnosis of HCC was 86.96%; the accuracy was 83.06%, while the sensitivity, the accuracy and the negative predictive value were improved to 91.86%, 84.68%, and 78.79% according to the combined detection of KAI1 and VEGF, respectively. CONCLUSIONS: A combined detection of KAI1 and VEGF may greatly improve the efficiency of diagnosis and form a reliable panel of diagnostic markers for HCC.
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Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Kangai-1 Protein/blood , Carcinoma, Hepatocellular/blood , Case-Control Studies , Gene Expression Regulation , Liver Diseases/genetics , Liver Neoplasms/blood , Vascular Endothelial Growth Factor A/blood , alpha-Fetoproteins/analysisABSTRACT
Objective To evaluate the infection of high-risk human papillomavirus (HPV) and the expression of tumor metastasis suppressor protein KAI1 in cervical cancer.Methods The expression of KAH,HPV16/18E6 and HPV16E7 proteins were analyzed by immunohistochemistry SP assay in 117 cases of paraffin-embedded cervical tissue,including 20 normal cerival tissue as control,58 intraepithelial neoplasia (CIN) and 39 cervical cancer.Results In normal cervical tissue,CIN and cervical cancer,the positive rate of KAI1 protein were respectively 90.0 ％ (18/20),72.4 ％ (42/58),25.6 ％ (10/39).There was significant differience among three gruop (P ＜ 0.01).The positive rate of HPV16/18E6 and HPV16E7 proteins were respectively 0 (0/20),31.0 ％ (18/58),41.0 ％ (16/39); 0 (0/20),34.5 ％ (20/58),64.1％ (25/39).There were significant differience among three gruops (P ＜ 0.01).There was no correlation between the expression of KAI1 and the infection of HPV (P =0.429).Expression of KAI1 was correlated to grade of differentiation,clinical stage and lymph node metastasis (P ＜ 0.05),but was not correlated to age (P ＞ 0.05).HPV infection was not correlated to the age,clinical stage,cell differentiation and lymph node metastasis (P ＞ 0.05).Conclusion The expression of KAI1 protein is down-regulated in cervical cancer,which is not associated with the infection of HPV.
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Objective To investigate the effects of KAll gene transfection on proliferation,migration,invasion and VEGF expression of pancreatic cancer MiaPaCa-2 cells under hypoxic condition,and explore possible mechanism.Methods The pcMV-KAI1 vector which contained the full length of KAI1 cDNA was transfected into pancreatic cancer cells MiaPaCa-2,and KAI1,VEGF C,VEGF A protein expressions were determined by Western blot.The proliferation of pancreatic cancer cells was evaluated by MTT method.Wound-healing assay and cell invasion assay were used to detect the migration and invasion of pancreatic cancer cells.The expression of VEGF C,VEGF A in supernatant of culture was measured by ELISA method.Results The expression of KAI1 protein in MiaPaCa-2 K transfected with KAI1 was significantly higher than that in nontransfected cells [(0.549 ± 0.021) vs 0,P＜0.05].The proliferation under hypoxic condition was not significantly different,but the migration distance was significantly shorter and the number of transmembrane cell was significantly decreased [(14.0 ± 5.8) vs (43.0 ± 14.4),P ＜ 0.05].The expression of VEGF-C in cell was significantly decreased [(0.218 ± 0.043) vs (0.745 ± 0.069),P ＜0.05],but the expression of VEGF-A was not significantly different; the expression of VEGF-C in cell culture supernatants was significantly decreased [(1236 ± 247) vs (2045 ± 221) pg/ml,P ＜ 0.01].Conclusions The migration,invasion ability of pancreatic cancer MiaPaCa-2 cells with KAll transfection under hypoxic condition is decreased,and the possible mechanism of inhibiting lymphatic metastasis is down-regulation of VEGF-C expression.
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ObjectiveTo study the change of autophagy of human pancreatic cancer cell MiaPaCa-2 before and after Ad5-KAI1 tranfection,and to investigate the possible mechanism.MethodsThe MiaPaCa-2 cells without KAI1 expression were infected with Ad5-KAI1 with KAI1 target gene,and Ad5-null was used as negative control,and parental cell was used as blank control.The formation of autophagosomes was observed by electromicroscopy.The green fluorescent protein-labeled light chain 3 (LC3) associations with autophagosome membranes was detected by confocal microscopy.PD98059,LY294002 were applied to pre-treat the cells.The expression levels of beclin 1,AKT,ERK,the phosphorylation of AKT and ERK protein and the ratio of LC3-Ⅱ to LC3- Ⅰ were detected by Western blotting.ResultsAfter 100 MOI Ad5-KAI1 infections for 24 h,the rate of cell expressing KAI1 protein reached (84.97 ±8.56)％,number of LC3 increased from 4 to 20; and swelling,degeneration of mitochondria was observed,and bilayer-like structure in cytoplasm was found.The expression of beclinl increased (1.4 ±0.3 ) folds,and the expression of LC3-Ⅱ/LC3- Ⅰ increased (8.00 ±2.78) folds.PI3K blockade LY294002 pretreatment significantly suppressed the phosphorylation of AKT of MiaPaCa-2 (2.756 vs 1.516),but it did not inhibit the increase of ratio of LC3-Ⅱ to LC3- Ⅰ(0.770 vs 1.403).ERK blockade PD98059 pretreatment not only significantly suppressed the phosphorylation of ERK of MiaPaCa-2 ( 1.637 vs 0.403 ),but also inhibit the up-regulation of beclin 1 protein expression ( 2.377 vs 1.150) and increase of ratio of LC3- Ⅱ to LC3- Ⅰ (2.225 vs 0.680).ConclusionsKAI1 can significantly induce autophagy of human pancreatic cell line MiaPaCa-2 through phosphorylation of ERK rather than AKT.
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Objective To explore the relationship between KAI1 gene expression in papillary thyroid carcinoma and clinicopathological features and prognosis. Methods KAI1 mRNA expression was detected by Real Time Polymerase Chain Reaction in 21 cases papillary thyroid carcinoma tissues and 21 cases adjacent normal tissues, as well as 7 cases benign thyroid disease tissues. KAI1 protein expression was detected by immunohistochemisty in 60 cases papillary thyroid carcinoma tissues and 20 cases thyroid adenoma tissues. Results KAI1 mRNA expression in papillary thyroid carcinoma was significantly higher than that in adjacent normal tissues (P ＜ 0. 05) and benign thyroid lesion tissues (P ＜ 0. 05). Positive expression rate of KAI1 protein was 68. 3% in papillary thyroid carcinoma and 25% in thyroid adenoma tissues. The difference was statistically significant (P ＜0. 01). In papillary thyroid carcinoma, positive expression rate of KAI1 protein in the group without lymph node metastasis was higher than that in group with lymph node metastasis (P＜0.05). There was no difference in positive expression rate of KAI1 protein for male or female patients (P ＞0. 05). KAI1 protein expression in papillary thyroid carcinoma was not related to patients' ages, tumor size, TNM staging or capsule invasion (P ＞ 0. 05). Conclusions The abnormal expression of KAI1 mRNA and protein is correlated to the genesis and progress of papillary thyroid carcinoma,which provides a clue for treatment and prognosis assessment of papillary thyroid carcinoma
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KAI1 is a recently identified metastasis suppressor gene located at human chromosome 11 p11.2. KAI1 protein is a member of the structurally distinct family of cell surface glycoprotein and belongs to transmembrane 4 protein superfamily. KAI1 expression is down-regulated in many metastatic tumor cells. Down-regulation of KAI1 expression also plays an important role in the genesis and development of gynecological tumor.
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AIM: To study the mRNA and protein expression of Kang ai1 (KAI1) tumor suppressor gene and to determine the relationship between KAI1 and invasiveness and metastasis of cervical cancer. METHODS: The expression of KAI1 metastasis suppressor was detected by immunohistochemistry in paraffin slides and by real-time quantitative polymerase chain reaction (RT-PCR) in fresh tissue. The samples included 20 cases of normal cervical tissues, 20 cases of cervical intraepithelial neoplasia (CIN) and 40 cases of cervical carcinoma. The results of the gene expression combined with the pathological and clinical data were also analyzed. RESULTS: The expression of KAI1 protein and mRNA was related to the tissue differentiation of cervix. The positive rates of KAI1 expression were the highest in the normal cervical tissue, the middle in CIN and the lowest in cervical carcinoma with significant difference among three groups (P<0.01). The expression of KAI1 protein was not related with the grade of CIN (P>0.05). However, both mRNA and protein expression of KAI1 were related to the differentiation and the clinical stages of cervical cancer (P<0.01) and also related to the metastasis of the cancer. The positive rates between the non-lymphatic metastasis and lymphatic metastasis (P<0.05) were significant different. Cox regression and logistic regression showed that the tissue differentiation, clinical stages, lymphatic metastasis and expression of KAI1 were all related factors with recurrence and prognosis of cervical cancer. CONCLUSION: The down-regulation of KAI1 tumor suppressor gene at both mRNA and protein levels is related to the differentiation, clinical stages and metastasis of cervical cancer, indicating that the expression of KAI1 is a prognostic factor for cervical cancer.
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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 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 evaluate the expression of KAII (CD82) gene inhibited by small interfering RNA (siRNA) in human pancreatic cancer cell line T3. Methods Four sequences of siRNA including A, B,C, D were designed, which were based on the KAI1 gene sequence using online RNA interfering designing software and lentivirus vector was built. Then they were used to transfect T3 cells by liposome 2000 and virus titer was determined. Empty vector containing siRNAd1 lentivrus particle ( MOI =5) was also used to infect T3 cells. The expression of CD82 mRNA was detected by real-time PCR. Results The expression of CD82 mRNA in normal control group, empty vector group, A group, B group, C group, D group were 1. 398 ±0.242,1. 311±0.048, 0. 664 + 0. 093, 0. 345 ± 0. 032, 0. 641 ± 0. 049 and 0. 147 ± 0. 049, respectively, the difference between the expression of CD82 mRNA in empty vector group and that of A, B, C, D groups was significant (P＜0.01 ). Conclusions RNAi was able to inhibit the expression of KAI1 gene CD82 in human pancreatic cancer cell line T3.
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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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Objective To observe the inhibitory effect on metastasis and growth of pancreatic cancer in mice by injection of KAI1 gene in vivo. Methods Pancreatic cancer cell line MiaPaCa Ⅱ was used to construct the nude mice models bearing tumors, then the mice were divided into normal saline group, Ad group and Ad-KAI1 group. Since the 10th days of model construction, the Ad-KAI1 was injected every 7 d and repeated twice, then the tumor size, the weight of liver, lung and their pathologic changes were evaluated. Results The tumor sizes were not significantly different between the three groups. The weight of lung and liver of Ad-KAI1 group was (0.366±0.041) g and (1. 35±0.21) g, respectively; the weight of lung and liver of Ad group was (0.57±0.065) g and (1.58±1.828) g, respectively; the weight of lung and liver of control group was (0.66±0.13)g and (1.95±0.344)g, respectively. The difference between Ad-KAI1 group and control group was significantly different (t = 5.984, P < 0. 05), and there was no significant difference between Ad group and control group (t=1.089, P > 0.05). The number of pulmonary, liver and lymph node metastasis in Ad-KAI1 group was (1±1), (2±1) and (2±2), respectively; in Ad group was (6±2), (5 ±1), (10±2), respectively; in control group was (7±2), (6±2), (11±3), respectively. The difference between Ad-KAI1 group and control group was significantly different (t = 7.44, 4.34, 8. 16, P < 0.05), while the difference between Ad group and control group was not significantly different (t=0.92, 0.64, 0.42, P >0.05). Conclusions KAI1 gene directly injected into tumors of nude mice may inhibit the growth and metastasis of pancreatic cancer.
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Objective To investigate the relationship between the expression of KAI1 mRNA and the clinicopathological parameters and prognostic outcome of patients with gastric Callcer. Methods The expressions of KAI1 mRNA in 70 samples of gastric cancer tissue and 18 samples of benign gastric lesion were detected by in situ hybridization.Results The positive rates of KAI1 mRNA expression in benign gastric lesion and gastric cancer tissue were 94%(17/18)and 31%(22/70),respectively.The expression of KAI1 mRNA was influenced by tumor difierentiation degree and the state of lymph node metastasis.The positive rate of KAI1 mRNA expression was gradually decreased as the increase of invasion depth and the tumor clinical stages.The 5-year survival rate of patients with positive expression of KAI1 mRNA WaS higher than these with negative expression of KAI1 mRNA.Conclmions The less and down-regulation of KAI1 gene expression may be involved in the occurrence and development of gastric cancer.KAI1 gene might be a valuable indicator for early diagnosis and predicting the malignancy and metastasis potential of gastric cancer and the prognosis of patients with gastric cancer.
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Objective: To investigate the association of EphA 2 and KAI 1 protein expressions with the occurrence, invasion, and metastasis of bladder transitional cell carcinoma tissues (BTCC). Methods: The expressions of EphA 2 and KAI 1 proteins were determined by immunohistochemical SP method in 88 cases of BTCC tissues and 76 cases of pericancerous normal bladder tissues. Results: The expression of EphA 2 protein was significantly higher in BTCC tissues than in adjacent normal tissues (P < 0.01). The expression of EphA 2 protein was gradually increased with the elevation of pathological grades of BTCC. The positive rate of EphA 2 expression was significantly higher in deeply infiltrating BTCC than superficially infiltrating BTCC (P < 0.05). It was significantly higher in the group with lymph node metastasis than those without lymph node metastasis (P < 0.05). The expression of KAI 1 protein was significantly lower in BTCC tissues than in adjacent normal tissues (P < 0.01). The expression of KAI 1 was gradually decreased with the elevation of pathological grades of BTCC. The positive rate of KAI 1 expression was significantly lower in deeply infiltrating BTCC than in superficially infiltrating BTCC (P < 0.05). It was significantly lower in the BTCC with lymph node metastasis than those without lymph node metastasis (P < 0.05). A significantly negative correlation was observed between the expression of EphA 2 and that of KAI 1 in BTCC tissues with lymph node metastasis (P < 0.05). Conclusion: Overexpression of EphA 2 and weak expression of KAI 1 may be involved in the tumorigenesis, infiltration, and migration of BTCC.