KAI1/CD82 gene and autotaxin-lysophosphatidic acid axis in gastrointestinal cancers.

The KAI1/CD82 gene inhibits the metastasis of most tumors and is remarkably correlated with tumor invasion and prognosis. Cell metabolism dysregulation is an important cause of tumor occurrence, development, and metastasis. As one of the important characteristics of tumors, cell metabolism dysregulation is attracting increasing research attention. Phospholipids are an indispensable substance in the metabolism in various tumor cells. Phospholipid metabolites have become important cell signaling molecules. The pathological role of lysophosphatidic acid (LPA) in tumors was identified in the early 1990s. Currently, LPA inhibitors have entered clinical trials but are not yet used in clinical treatment. Autotaxin (ATX) has lysophospholipase D (lysoPLD) activity and can regulate LPA levels in vivo. The LPA receptor family and ATX/lysoPLD are abnormally expressed in various gastrointestinal tumors. According to our recent pre-experimental results, KAI1/CD82 might inhibit the migration and metastasis of cancer cells by regulating the ATX-LPA axis. However, no relevant research has been reported. Clarifying the mechanism of ATX-LPA in the inhibition of cancer metastasis by KAI1/CD82 will provide an important theoretical basis for targeted cancer therapy. In this paper, the molecular compositions of the KAI1/CD82 gene and the ATX-LPA axis, their physiological functions in tumors, and their roles in gastrointestinal cancers and target therapy are reviewed.

Metabolomic Detection Between Pancreatic Cancer and Liver Metastasis Nude Mouse Models Constructed by Using the PANC1-KAI1/CD82 Cell Line.

Background: Pancreatic cancer (PC) has a poor prognosis and is prone to liver metastasis. The KAI1/CD82 gene inhibits PC metastasis. This study aimed to explore differential metabolites and enrich the pathways in serum samples between PC and liver metastasis nude mouse models stably expressing KAI1/CD82. Methods: KAI1/CD82-PLV-EF1α-MCS-IRES-Puro vector and PANC1 cell line stably expressing KAI1/CD82 were constructed for the first time. This cell line was used to construct 3 PC nude mouse models and 3 liver metastasis nude mouse models. The different metabolites and Kyoto encyclopedia of genes and genomes (KEGG) and human metabolome database (HMDB) enrichment pathways were analyzed using the serum samples of the 2 groups of nude mouse models on the basis of untargeted ultra-performance liquid chromatography-tandem mass spectrometry platform. Results: KAI1/CD82-PLV-EF1α-MCS-IRES-Puro vector and PANC1 cell line stably expressing KAI1/CD82 were constructed successfully, and all nude mouse models survived and developed cancers. Among the 1233 metabolites detected, 18 metabolites (9 upregulated and 9 downregulated) showed differences. In agreement with the literature data, the most significant differences between both groups were found in the levels of bile acids (taurocholic acid, chenodeoxycholic acid), glycine, prostaglandin E2, vitamin D, guanosine monophosphate, and inosine. Bile recreation, primary bile acid biosynthesis, and purine metabolism KEGG pathways and a series of HMDB pathways (P < .05) contained differential metabolites that may be associated with liver metastasis from PC. However, the importance of these metabolites on PC liver metastases remains to be elucidated. Conclusions: Our findings suggested that the metabolomic approach may be a useful method to detect potential biomarkers in PC.

KAI1(CD82) is a key molecule to control angiogenesis and switch angiogenic milieu to quiescent state.

BACKGROUND: Little is known about endogenous inhibitors of angiogenic growth factors. In this study, we identified a novel endogenous anti-angiogenic factor expressed in pericytes and clarified its underlying mechanism and clinical significance. METHODS: Herein, we found Kai1 knockout mice showed significantly enhanced angiogenesis. Then, we investigated the anti-angiogenic roll of Kai1 in vitro and in vivo. RESULTS: KAI1 was mainly expressed in pericytes rather than in endothelial cells. It localized at the membrane surface after palmitoylation by zDHHC4 enzyme and induced LIF through the Src/p53 pathway. LIF released from pericytes in turn suppressed angiogenic factors in endothelial cells as well as in pericytes themselves, leading to inhibition of angiogenesis. Interestingly, KAI1 had another mechanism to inhibit angiogenesis: It directly bound to VEGF and PDGF and inhibited activation of their receptors. In the two different in vivo cancer models, KAI1 supplementation significantly inhibited tumor angiogenesis and growth. A peptide derived from the large extracellular loop of KAI1 has been shown to have anti-angiogenic effects to block the progression of breast cancer and retinal neovascularization in vivo. CONCLUSIONS: KAI1 from PC is a novel molecular regulator that counterbalances the effect of angiogenic factors.

Role of a metastatic suppressor gene KAI1/CD82 in the diagnosis and prognosis of breast cancer.

Globally, breast cancer is the most common type of cancer in females and is one of the leading causes of cancer death in women. The advancement in the targeted therapies and the slight understanding of the molecular cascades of the disease have led to small improvement in the rate of survival of breast cancer patients. However, metastasis and resistance to the current drugs still remain as challenges in the management of breast cancer patients. Metastasis, potentially, leads to failure of the available treatment, and thereby, makes the research on metastatic suppressors a high priority. Tumor metastasis suppressors are several genes and their protein products that have the capability of arresting the metastatic process without affecting the tumor formation. The metastasis suppressors KAI1 (also known as CD82) has been found to inhibit tumor metastasis in various types of solid cancers, including breast cancer. KAI1 was identified as a metastasis suppressor that inhibits the process of metastasis by regulating several mechanisms, including cell motility and invasion, induction of cell senescence, cell-cell adhesion and apoptosis. KAI1 is a member of tetraspanin membrane protein family. It interacts with other tetraspanins, chemokines and integrins to control diverse signaling pathways, which are crucial for protein trafficking and intracellular communication. It follows that better understanding of the molecular events of such genes is needed to develop prognostic biomarkers, and to identify specific therapies for breast cancer patients. This review aims to discuss the role of KAI1/CD82 as a prognosticator in breast cancer.

Down Regulation of KAI1/CD82 in Lymph Node Positive and Advanced T-Stage Group in Breast Cancer Patients.

BACKGROUND: Metastasis represents a deadly aspect of any cancer including breast cancer, given its high prevalence; treatment of metastatic breast cancer remains a clinically unmet need, which necessitates the exploration of metastasis suppressor genes (MSGs). KAI-1/CD82 is an important member of MSGs; the role of KAI1 has been well explored in prostate cancer, however its role in breast cancer is not fully explored and in fact the results of breast cancer studies are contentious. Thus, the present study aimed to investigate expression of KAI1 at both transcriptional and translational levels in the tissue of breast cancer patients and benign breast disease. Further, we analysed the relationship between expression levels of KAI1 and clinicopathological parameters in breast cancer patients. MATERIALS AND METHODS: mRNA expression was studied by Real time PCR and protein expression was analyzed by both Western blot and Immunohistochemistry. RESULTS: The results of the study indicate that KAI1 expression was remarkably decreased in breast cancer both at the gene and the protein levels (P < 0.05) compared to benign breast disease. In addition, KAI1 expression levels were strongly associated with axillary lymph node status and advanced T stage (p < 0.05), however no association was found with tumor grade, age, menopausal status and receptor status like ER, PR and Her2. CONCLUSION: Low expression of KAI1 might be helpful for predicting the lymph node metastasis and T staging, thus predicts malignant prognosis of breast cancer.
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Differential tumor biological role of the tumor suppressor KAI1 and its splice variant in human breast cancer cells.

The tetraspanin and tumor suppressor KAI1 is downregulated or lost in many cancers which correlates with poor prognosis. KAI1 acts via physical/functional crosstalk with other membrane receptors. Also, a splice variant of KAI1 (KAI1-SP) has been identified indicative of poor prognosis. We here characterized differential effects of the two KAI1 variants on tumor biological events involving integrin (αvß3) and/or epidermal growth factor receptor (EGF-R). In MDA-MB-231 and -435 breast cancer cells, differential effects were documented on the expression levels of the tumor biologically relevant integrin αvß3 which colocalized with KAI1-WT but not with KAI1-SP. Cellular motility was assessed by video image processing, including motion detection and vector analysis for the quantification and visualization of cell motion parameters. In MDA-MB-231 cells, KAI1-SP provoked a quicker wound gap closure and higher closure rates than KAI1-WT, also reflected by different velocities and average motion amplitudes of singular cells. KAI1-SP induced highest cell motion adjacent to the wound gap borders, whereas in MDA-MB-435 cells a comparable induction of both KAI1 variants was noticed. Moreover, while KAI1-WT reduced cell growth, KAI1-SP significantly increased it going along with a pronounced EGF-R upregulation. KAI1-SP-induced cell migration and proliferation was accompanied by the activation of the focal adhesion and Src kinase. Our findings suggest that splicing of KAI1 does not only abrogate its tumor suppressive functions, but even more, promotes tumor biological effects in favor of cancer progression and metastasis.

Effect of KAI1/CD82-expressing EPCs on lung metastasis of a xenograft mouse model of human nasopharyngeal carcinoma / 临床与实验病理学杂志

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.

Evaluation of imatinib mesylate (Gleevec) on KAI1/CD82 gene expression in breast cancer MCF-7 cells using quantitative real-time PCR

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

Clinical significance of KAI1/CD82 protein expression in nasopharyngeal carcinoma.

The aim of this study was to investigate KAI1/CD82 protein expression in human nasopharyngeal carcinoma (NPC) cell lines and human NPC tissues. Immunohistochemistry and western blot analysis were used to detect the localization and expression levels of the KAI1/CD82 protein in five human NPC cell lines. Immunohistochemistry was also conducted to detect the expression of the KAI1/CD82 protein in 70 NPC tissues and 30 non-neoplastic nasopharyngeal tissues. The levels of KAI1/CD82 protein expression were found to decrease as the metastatic potential of cells increased. The expression rate of KAI1/CD82 protein in the NPC tissues (44.3%) was significantly lower than that in the non-neoplastic nasopharyngeal tissues (70.0%) (P<0.05). KAI1/CD82 protein expression in the NPC tissues was not associated with clinical parameters, including gender, age, histological type and T stage, and the positive expression of KAI1/CD82 decreased with increased N staging. The level of KAI1/CD82 protein expression was increased in different human NPC cell lines. The KAI1/CD82 gene was highly expressed in cells with low metastatic potential, while low expression was observed in cells with a high metastatic potential. In addition, the KAI1/CD82 gene was expressed at low levels in nasopharyngeal carcinoma tissues, while high expression was identified in non-neoplastic nasopharyngeal tissues, and was associated with lymph node metastasis. These results indicated that the KAI1/CD82 gene may be involved in the occurrence, development and metastasis of nasopharyngeal carcinoma.

Alternative splicing of KAI1 abrogates its tumor-suppressive effects on integrin αvß3-mediated ovarian cancer biology.

Loss or downregulation of the tumor-suppressor KAI1 correlates with poor cancer patient prognosis. KAI1 functions by interacting with other proteins, including integrin cell adhesion and signaling receptors. We previously showed that KAI1 physically and functionally crosstalks with the tumor-biologically relevant integrin αvß3, thereby suppressing ovarian cancer cell migration and proliferation. Interestingly, in metastases, a KAI1 splice variant had been identified, indicating poor patient prognosis. Thus, we here characterized differential effects of the two KAI1 proteins upon their cellular restoration. Opposite to KAI1, KAI1-splice reduced αvß3-mediated cell adhesion, thereby inducing cell migration. This was accompanied by elevated αvß3 levels and drastically elevated focal adhesion kinase activation, however, without any obvious colocalization with αvß3, as observed for KAI1. Moreover, codistribution of KAI1 with the cell/cell-adhesion molecule E-cadherin was abrogated in KAI1-splice. Whereas KAI1 diminished cell proliferative activity, KAI1-splice prominently enhanced cell proliferation concomitant with elevated transcription and cell-surface expression of the epidermal growth factor receptor. Thus KAI1-splice does not only counteract the tumor-suppressive actions of KAI1, but - beyond that - promotes αvß3-mediated biological functions in favor of tumor progression and metastasis.

Expression of KAI1/CD82 and CD44 v6 in human laryngeal squamous cell carcinoma and their clinical significance / 临床与实验病理学杂志

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.

Expression and significance of KAI1/CD82 and CD44v6 in human laryngeal squamous cell carcinoma / 安徽医科大学学报

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.

KAI1/CD82 and cyclin D1 as biomarkers of invasion, metastasis and prognosis of laryngeal squamous cell carcinoma.

OBJECTIVE: This study aimed to investigate the expressions and significance of KAI1/CD82 and cyclin D1 in laryngeal squamous cell carcinoma (LSCC). METHODS: Real-time quantitative PCR (Q-PCR) and Western blot assay were employed to detect the expressions of KAI1/CD82 and cyclin D1 in the laryngeal tissues of 86 LSCC patients, 32 patients with laryngeal polyp and 38 patients with laryngeal leukoplakia, and the influence of both proteins on the clinicopathological features and survival of LSCC patients. RESULTS: The changes in mRNA and protein expressions of KAI1/CD82 and cyclin D1 were consistent in three groups, and the expressions of KAI1/CD82 and cyclin D1 were significantly different among three groups (P<0.01 or <0.05). The KAI1/CD82 expression in patients with TNM stage III-IV LSCC, poorly differentiated LSCC, clinical stage III-IV LSCC or lymph node metastasis was markedly lower than that in those with TNM stage I-II LSCC, well differentiated LSCC, clinical stage I-II LSCC or no lymph node metastasis (P<0.01 or <0.05). However, there was no marked difference in KAI1/CD82 expression between males and females and among patients in different age groups (P>0.05). In LSCC patients positive for KAI1/CD82 protein expression, the median survival time was 76 months, which was significantly longer than that in LSCC patients negative for KAI1/CD82 protein expression (48 months; X(2)=16.293, P=0.000). The Cyclin D1 expression in patients with TNM stage III-IV LSCC, poorly differentiated LSCC, or clinical stage III-IV LSCC was dramatically higher than that in patients with TNM stage I-II LSCC, well differentiated LSCC, or clinical stage I-II LSCC (P<0.01 or <0.05). However, no marked difference was noted in cyclin D1 expression between males and females, among patients in different age groups and between patients with and without lymph node metastasis (P>0.05). In LSCC patients positive for cyclin D1 protein expression, the median survival time was 40 months, which was markedly shorter than that in LSCC patients negative for cyclin D1 protein expression (X(2)=9.517, P=0.02). In LSCC patients, there was a negative correlation between KAI1/CD82 expression and cyclin D1 expression (X(2)=7.86, P<0.01). CONCLUSION: KAI1/CD82 affects cell cycle. Both KAI1/CD82 and cyclin D1 are involved in the occurrence and development of LSCC, and may provide clinical information for evaluation of invasiveness, metastasis and prognosis of LSCC. Thus, KAI1/CD82 and cyclin D1 may serve as markers for determination of invasiveness, metastasis and prognosis of LSCC.

Expression and significance of KAI1/CD82,E-cadherin and β-catenin in endometrial carcinoma / 中国基层医药

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.

Hypoxia-induced enhancement of cell invasiveness in SMMC7721 hepatocellular carcinoma cells / 药物分析学报

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.

Hypoxia-induced enhancement of cell invasiveness in SMMC7721 hepatocellular carcinoma cells / 西安交通大学学报·英文版

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.

Correlation of KAI1/CD82 and laminin receptor in cholangiocarcinoma / 中华消化外科杂志

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.

Expression of KAI1/CD82 and MRP-1/CD9 in Transitional Cell Carcinoma of Bladder / 华中科技大学学报（医学）（英德文版）

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.

Expression and significance of KAI1/CD82 gene in non-small cell lung cancer / 第三军医大学学报

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

Expression and significance of KAI1/CD82 and E-Cadherin in Human squamous cervical carcinoma / 西安交通大学学报(医学版)

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.