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ObjectiveTo investigate the expression and significance of CDX2,Ki-67 in adenoma and colorectal adenocarcinoma,and the correlation between CDX2 and Ki-67.MethodsThe expression of CDX2 and Ki-67 was evaluated in the colorectal adenocarcinoma,adenoma and normal colorectal mucosa as control subjects by immunohistochemistry.ResultsThe magnitude of CDX2 were negatively correlated with the level of dysplasia in adenoma(rs=-0.38,P =0.02),and negatively correlated with differentiation,lymph node metastasis,diversion and Dukes stage of cancer in colorectal adenocarcinoma(rs=-0.49,rs=-0.37,rs =- 0.38,rs =-0.37,P =0.01).The expression and relativity of Ki-67 in the samples were contrary to the CDX2.The levels of CDX2 and Ki-67 expression had significant difference between the adenoma and adenocarcinoma,and showed negatively correlation in this two type tissues (rs=-0.69,P =0.00; rs =-0.40,P =0.00).ConclusionsCDX2 may be used as an effective marker to evaluate malignancy degree and prognosis of large bowel neoplasm patient.The levels of Ki-67 expression in colorectal adenocarcinoma are correlated with malignancy degree and clinical stage.The expression of CDX2 is negatively correlated with Ki-67.Combined detection of CDX2 and Ki-67 may be helpful for the judgment of colorectal tumor biological characters.
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Objective To explore the effect of vitamin D receptor (VDR) in intestinal tumor development and the relationship between VDR and β-catenin signaling pathway. Methods The interaction of vitamin D receptor and β-catenin were detected by co-immunoprecipitation assay after human colonic carcinoma cells SW480 were treated with vitamin D in vitro for 4 hours. The expression of E-cadherin protein was detected by Western blot after treated for 24 hours. To compare APCmin/+VDR-/- and APCmin/+ mice in vivo, the expression of VDR,β-catenin and BrdU proteins in intestinal tumor were determined by immunohistochemistry. The expression of β-catenin protein in tumor and adjacency intestinal was further determined by Western blot. Results After SW480 cells were treated with vitamin D, vitamin D receptor and β-catenin protein showed binding, the expression of E-cadherin protein further increased (Gray value the control group 145.57±4.21,Gray value of the experimental group 109.35±3.56,t＝32.63,P＜0.05). Immunostaining and Western blot detection（Gray value 166.47±2.36） showed a marked increase of β-catenin level(Gray value 140.51±2.57) in APCmin/+VDR-/- tumor compared to APCmin/+ tumor(145.41±3.62,182.35±3.24,t＝2.65,4.36,P＜0.05). Conclusions The role of vitamin D suppressing intestinal tumor may be achieved through VDR affectingβ-catenin signaling pathway.
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Objective To observe the solo-allied expression of Survivin, Smad4/dpc4 and APC gene, and study the relationship between the three genes and biological behavior of colorectal cancer. Methods The expressions of Survivin, Smad4/dpc4 and APC gene were detected by SP immunohistochem-istry among the cases from 40 eu-intestine ,80 large intestinal adenoma and 80 CRC. Results The positive rate of survivin protein in the eu-intestine, the large intestinal adenoma and CRC was 0,35.0% ,75.0% , respectively. The positive rate of Smad4/dpc4 protein was 100% , 95. 0% , 78. 8% , and the positive rate of APC protein was 100% ,80.0% ,45.0% , respectively. In the eu-intestine, APC + Smad4/dpc4 Z- expressed in 40 cases, with the incidence of 100%. In the large intestinal adenoma, APC + Smad4 expressed in 38 patients, with the incidence of 47. 5% , and the three genes expressed in 29 patients with the incidence of 23. 8%. In the CRC, two genes expressed in 57 patients, with the incidence of 71. 3% , and three genes expressed in 28 patients, with the incidence of 35.0%. Conclusion The detection of survivin was a new indicator in early diagnosis of CRC. It was significant in the diagnosis of CRC that energetic search for the positive rate level realm of survivin. The catastrophe or absence of Smad4/dpc4 gene not only induced the genesis of CRC but also encouraged its growth. Smad4/dpc4 was ant- carcinomatous gene intimately correlated to the CRC. Detection of APC gene had very important significance, it could be helpful to conduct the research of tumorous aetiology, nosogenesis and early diagnosis. The allied detection of Survivin, Smad4/dpc4, APC gene played a very important role in early diagnosing and healing the CRC.
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Objective This study was to explore the inhibitory effect of shRNA-VEGF - C on growth of human colon cancer cell line Lovo in vitro and vivo. Methods Recombinant VEGF-C short hairpin RNA (shRNA) plasmid was constructed and transfected into Lovo cells. The expression of VEGF-C was detected at mRNA and protein levels by real-time reverse transcription-polymerase chain reaction (RT-PCR). In vivo study, xenograft tumors were established by injecting LOVO cells into nude mice, then shR-NA-VEGF-C were injected into the tumors, the tumor volume and weight and the incidences of lymph node metastasis were detected. Immunohistochemical staining was used to detect the lymphatic microvessel density of colon cancer tissues. Results After transfection of shRNA-VEGF-C, the mRNA of VEGF-C in Lovo cells were down-regulated. Four weeks after injection, the tumor volume and tumor weight in VEGF-C-shR-NA group were significantly smaller than that in empty plasmid group and NS group [(324. 9 ± 64. 8 ) mm3 vs. (553.5±90. 1)mm3 and (570. 1±85.4)mm3; (3.01 ±0.55)g vs (4.65 ±0.65)g and (4.75 ±0. 75)g]. The incidences of lymph node metastasis (30. 1% ) were significantly inhibited compared with empty plasmid group (50. 2% ) and normal saline group (53. 1% ). In shRNA-VEGF-C group, and microlymphatic density (15.5 ± 6. 90) was also decreased compared with empty plasmid group (24. 18 ±6. 45 ), and normal saline group (29. 59 ± 8. 21 ) ( all P <0. 01 ). Conclusion shRNA-VEGF-C can inhibit the growth of LOVO cells in vitro and vivo. VEGF-C may inhibit the lymph node metastasis of colon cancer by suppressing lymphangiogenesis.