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1.
International Journal of Laboratory Medicine ; (12): 400-402,407, 2018.
Article in Chinese | WPRIM | ID: wpr-692677

ABSTRACT

Objective To explore the change and clinical significance of the serum carcinoembryonic antigen (CEA)and carbohydrate antigen 724(CA724)in patients with rectal cancer before and after neoadjuvant ra-diotherapy and chemotherapy.Methods The serum levels of CEA and CA724 of 30 patients with rectal carci-noma were detected by electrochemiluminescence method and were compared with those in 30 healthy people. Results The serum levels of CEA and CA724 in rectal carcinoma patients before neoadjuvant radiotherapy and chemotherapy were significantly higher than those in the healthy people,the difference was statistically significant(P<0.05).The serum levels in complete remission and partial remission patients after eight-week neoadjuvant radiotherapy and chemotherapy were significantly lower than those before treatment,the differ-ence was statistically significant(P<0.05),and the reduction levels were obviously higher than those in the stable group,the difference was statistically significant(P< 0.05).The CEA and CA724 levels in the stable treatment patients were also lower than those of before neoadjuvant radiotherapy and chemotherapy,the difference was statistically significant(P<0.05).The serum levels in the progression group were higher than those of before treatment(P<0.05).The serum levels of CEA and CA724 before neoadjuvant radiotherapy and chemotherapy existed a positive correlation(r=0.862,P=0.000).Conclusion The serum levels of CEA and CA724 in rectal cancer are highly expressed,suggesting that both of them are closely related to the occur-rence and development of rectal carcinoma,the measurement of the serum level changes of CEA and CA724 in patients with rectal cancer before and after treatment contributes to estimate the efficacy of neoadjuvant radio-therapy and chemotherapy and tumor progression.

2.
Chinese Journal of Postgraduates of Medicine ; (36): 735-737, 2017.
Article in Chinese | WPRIM | ID: wpr-618160

ABSTRACT

Objective To investigate the expression of circulating tumor cells (CTC) in peripheral blood of patients with different stages of colorectal cancer (CRC), and to evaluate its significance in early diagnosis of colorectal cancer metastasis. Methods Sixty patients with CRC (42 inⅡ-Ⅲstage and 18 in IV stage ) and 30 patients with benign rectal disease were recruited from January 2014 to December 2015. The CTC in peripheral blood was purified with Immunomagnetic Separation Technologie, and detected by immunofluorescence in situ hybridization (imFISH). The serum levels of CEA were detected by electrochemiluminescence method meanwhile. The correlation between CTC and CEA was analyzed. Results CTC positive rates in CRC patients were significantly higher than those in benign rectal disease controls. CTC positive rates inⅣstage were significantly higher than those inⅡ-Ⅲ stage. The expression of CTC was significantly correlated with CEA (r = 0.6652, P < 0.01). Conclusions The expression of CTC in CRC patients is significantly higher than that in benign rectal disease control group. It is closely related to clinical stages. Detection of peripheral blood CTC has important clinical significance in the early diagnosis of CRC metastasis.

3.
The Journal of Practical Medicine ; (24): 1745-1748, 2016.
Article in Chinese | WPRIM | ID: wpr-494491

ABSTRACT

Objective To investiagate cell apoptosis and expressions of Bax,Bcl-2 andCaspase-3 in gambogic acid-treated colorectal cancer cells. Methods SW480/LOVO colorectal cancer cells were treated by gambogic acid. Cell Counting Kit-8 assay (CCK-8) was used to test cell proliferation. Microscopy was used to check the morphological changes. Immunofluorescence staining technique was used to detect cell apoptosis. Expressions of Bax,Bcl-2 and Caspase-3 protein were detected by Western blot assay. Results Gambogic acid inhibited the proliferation of SW480/LOVO in a dose and time-dependent manner. Gambogic acid could induce cell apoptosis. Gambogic acid increased expressions of Caspase-3 and Bax, increased the ratio of Bax/Bcl-2, and decreased Bcl-2 protein expression. Conclusion Gambogic acid can inhibit proliferation and induce apoptosis of SW480LOVO cells, with the mechanism of up-regulation of Bax/Bcl-2 and activation of Caspase-3.

4.
Chinese Journal of Gastrointestinal Surgery ; (12): 695-701, 2016.
Article in Chinese | WPRIM | ID: wpr-323587

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect and its possible mechanism of interleukin-17 (IL-17) on invasion and metastasis of human colon cancer cells.</p><p><b>METHODS</b>IL-17 was added into the culture media of human colon cancer cells SW480 and LOVO. Cells were divided into 4 groups: SW480 control group (SW480 cells), LOVO control group (LOVO cells), SW480 experiment group (50 μg/L IL-17+SW480 cells), and LOVO experiment group (50 μg/L IL-17+LOVO cells). Cell growth was measured by CCK-8 assay. The proliferation rate(%)=[(Aexperiment group-Ablank)/(Acontrol group-Ablank)]×100%). The ability of cell invasion and migration was measured by transwell assay. Real time-PCR was used to detect mRNA expression of VEGF and MMP-9. Western blot was performed to detect protein expression of STAT3, p-STAT3, VEGF and MMP-9. Enzyme-linked immunosorbent assay (ELISA) was applied to measure the protein content of VEGF and MMP-9 in the supernatant.</p><p><b>RESULTS</b>After cultivation for 24, 48 and 72 hours, CCK-8 assay revealed that the proliferation rate of SW480 was 1.18%±0.07%, 1.42%±0.09%, and 1.62%±0.08%; the proliferation rate of LOVO was 1.13%±0.02%, 1.32%±0.05% and 1.73%±0.02% in experiment group. Transwell experiments showed that after cultivation with IL-17 for 24 hours, number of invasion cell in experimental groups (SW480: 34.00±0.45, LOVO: 41.60±0.51) was higher as compared to corresponding control groups (SW480: 4.53±0.14; LOVO: 3.67±0.33) with significant differences (SW480: t=-76.026, P=0.001; LOVO: t=-81.580, P=0.005). The number of migration cell in experimental groups (SW480: 36.40±0.51, LOVO: 46.40±0.68) was higher as compared to corresponding control groups (SW480: 7.83±0.69; LOVO: 6.67±0.48) with significant differences (SW480: t=-51.542, P=0.003; LOVO: t=-49.265, P=0.005). Real-time PCR results revealed that after cultivation with IL-17 for 24 hours, VEGF and MMP-9 mRNA relative expression levels in experimental groups (SW480: VEGF:1.53±0.12, MMP-9: 2.44±0.23; LOVO: VEGF: 2.96±0.35, MMP-9: 3.38±0.55) were higher than those in control groups (both 1) with significant differences (VEGF: t=3.799, P=0.043; MMP-9: t=5.254, P=0.039). Western blot illustrated that after cultivation with IL-17 for 24 hours, STAT3, p-STAT3, VEGF and MMP-9 proteins relative expression levels in experimental groups were significantly higher that those in control groups (SW480:STAT3: t=3.233, P=0.023; p-STAT3: t=3.954, P=0.032; VEGF: t=3.201, P=0.025; MMP-9: t=3.154, P=0.029; LOVO: STAT3: t=3.788, P=0.012; p-STAT3: t=2.662, P=0.040; VEGF: t=4.118, P=0.035; MMP-9: t=4.268, P=0.030). ELISA indicated that content of VEGF and MMP-9 in the supernatant of experimental groups (SW480: VEGF 5 491.41±63.22, MMP-9: 21.43±1.35. LOVO: VEGF: 8 631.46±129.59, MMP-9: 178.32±3.20) were higher than those in control groups (SW480: VEGF:4 456.32±87.56, MMP-9:18.57±2.44. LOVO: VEGF: 8 122.38±108.66, MMP-9: 163.22±6.89) with significant differences (SW480: VEGF: t=6.993, P=0.037; MMP-9: t=5.587, P=0.040. LOVO: VEGF: t=7.013, P=0.044; MMP-9: t=6.762, P=0.043).</p><p><b>CONCLUSION</b>IL-17 may be able to activate STAT3 signal transduction pathway in vitro through up-regulation of VEGF and MMP-9 expression, thereby enhancing the invasion and migration of colon cancer SW480 and LOVO cells.</p>


Subject(s)
Humans , Cell Cycle , Cell Line, Tumor , Cell Movement , Cell Proliferation , Colonic Neoplasms , Pathology , Interleukin-17 , Pharmacology , Matrix Metalloproteinase 9 , Metabolism , Neoplasm Invasiveness , Real-Time Polymerase Chain Reaction , STAT3 Transcription Factor , Metabolism , Signal Transduction , Up-Regulation , Vascular Endothelial Growth Factor A , Metabolism
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