ObjectiveTo study the relationship between the expression of sialyl Lewisx (SLeX) antigen and CD44v6 products and biological behaviors in cholangiocarcinomas. MethodsThe expression of SLeX and CD44v6 in 43 cases of cholangiocarcinoma tissue was respectively investigated by catalyzed signal amplification immunohistochemical technique.The relationship between expression of SLeX and CD44v6 and the clinicopathological factors of cholangiocarcinoma was analyzed.ResultsThe positive expression rate of SLeX and CD44v6 in cholangiocarcinoma was 67.4% and 62.8% respectively,which was significantly higher than that in control group (20.0%,P＜0.05).The high level expression of SLeX and CD44v6 were correlated with the TNM phase, differentiation degree,metastasis to lymph nodes and viscera in cholangiocarcinoma (P＜0.05). Moreover,there was a positive correlation between the SLeX and CD44v6 expression in cholangiocarcinoma (r=0.49,P＜0.001).Conclusion Expression of SLeX and CD44v6 could be helpful in predicting the biological behavior and prognosis of cholangiocarcinoma.
Carcinoembryonic antigen (CEA)was measured with ABC immunohistochemistry method in fourty-one gastric cancer tissues and sixty-six tissue from normal stomach and gastric benign lesions. The study revealed that the reactive signals in the former were ber than those in the latter. Simultaneously, CEA localized mainly in the cytoplasm or stroma in the cancerous tissue, but in normal gastric tissue or benign gastric lession, CEA distributed mainly in the margin of gland with gastric depression or membranous type. The result also revealed that the distribution patterns of ECA were linked with the cell growth types and infiltrating of gastric cancer. The authors consider that the expression state of CEA in gastric cancer is correlated with its biological behavior, and distribution patterns of CEA are more clinically significant than reactive intensities in the tissue. Patients have different prognosis with different CEA distribution patterns in tissue though their pathological types and TNM stages are the same.
Objective To detect the expressions of RhoA and Snail in gastric cancer tissues， and explore the relati-onship of these expressions to the biological behavior of the gastric cancer. Methods The expressions of RhoA and Snail protein in the paraffin-embedded specimens of 189 gastric cancer patients were detected by immunohistochemical method. The relationships of their expressions to clinicopathologic features of gastric cancer or survival， and the relevance of RhoA expression and Snail expression were analyzed. Results ① The expressions of RhoA and Snail protein in the gastric cancer tissues were significantly higher than those in the paraneoplastic tissue （RhoA：P=0.008；Snail：P=0.000） and the normal gastric mucosa tissue （RhoA：P=0.010；Snail：P=0.000）；The expression of RhoA had no significant difference between the paraneoplastic tissue and the normal gastric mucosa tissue （P=0.782）， however， the expression of Snail in the paraneoplastic tissue was significantly higher than that in the normal gastric mucosa tissue （P=0.001）. ② The expression of RhoA in the gastric cancer tissue was associated with TNM staging and Lauren type （P＜0.05）， but it was not associated with tumor diameter， lymph node metastasis， or differentiation degree （P＞0.05）. The expression of Snail in the gastric cancer tissue was associated with tumor diameter， lymph node metastasis， differentiation degree， TNM staging， or Lauren type （P＜0.05）. The expressions of RhoA and Snail in the gastric cancer tissue were not associated with patients’ gender and age （P＞0.05）. ③ The expression of RhoA protein was significantly positi-vely correlated with Snail protein in the gastric cancer（rs=0.203， P=0.005）. ④ The TNM staging of tumor， RhoA and Snail expressions， and lymph node metastasis were all the independent prognostic factors of postoperative gastric cancer patients （P＜0.05）. Conclusions RhoA and Snail proteins express in gastric cancer tissues， and involves in gastric carcinogenesis and the development process， and RhoA/Snail signaling pathway may play an important role in invasion and metastasis of gastric cancer.
Objective To investigate the effect of microRNA-584-5p (miR-584-5p) on the biological behavior (proliferation, migration and invasion) of breast cancer cells and its mechanism. Methods Human normal breast epithelial cells MCF10A and breast cancer cells MDA-MB-231, SK-BR-3 and MCF-7 were selected; take MCF-7 cells in logarithmic growth phase, transfect them with LipofectamineTM 2000 transfection kit, and divide them into seven groups: blank group (untransfected MCF-7 cells), mimic-negative control (mimic-NC) group (transfected mimic-NC), miR-584-5p mimic group (transfected miR-584-5p mimic), pcDNA group [transfected with overexpression of matrix metalloproteinase-14 (MMP-14) pcDNA3.1 plasmid negative control (pcDNA3.1)], MMP-14 group [transfected with overexpression of MMP-14 pcDNA3.1 plasmid (pcDNA3.1-MMP-14)], mimic-NC+MMP-14 group (co-transfected with mimic NC and pcDNA3.1-MMP-14), and miR-584-5p mimic+MMP-14 group (co-transfected with miR-584-5p mimic and pcDNA3.1-MMP-14). The mRNA expression levels of miR-584-5p in MCF10A, MDA-MB-231, SK-BR-3 and MCF-7 cells and the expression levels of miR-584-5p and MMP-14 mRNA of MCF-7 cell in each group were detected by fluorescence quantitative PCR. The protein expressions of MMP-14 of MCF-7 cell in each group were detected by Western blotting. The proliferation, migration and invasion of MCF-7 cell in each group were detected by cell counting kit - 8 (CCK-8), scratch test and Transwell test. The targeting relationship between miR-584-5p and MMP-14 was detected by double luciferase reporter gene assay. Results Compared with the human normal mammary epithelial cells MCF10A, the expression levels of miR-584-5p in breast cancer cells MDA-MB-231, SK-BR-3 and MCF-7 were decreased (P<0.05), and the expression level of miR-584-5p in MCF-7 cells was the lowest. Compared with the blank group and the mimic-NC group, the expression level of miR-584-5p of MCF-7 cells in the miR-584-5p mimic group was increased, and the expression levels of MMP-14 mRNA and protein, proliferation activity, scratch healing rate and invasive cell number were decreased or reduced (P<0.05). Compared with the blank group and the pcDNA group, the expression levels of MMP-14 mRNA and protein, proliferation activity, scratch healing rate and invasive cell number of MCF-7 cells in the MMP-14 group were increased (P<0.05). Compared with the MMP-14 group and the mimic-NC+MMP-14 group, the expression level of miR-584-5p of MCF-7 cells in the miR-584-5p mimic+MMP-14 group was increased, the expression levels of MMP-14 mRNA and protein, proliferation activity, scratch healing rate and invasive cell number were decreased or reduced (P<0.05). The expression levels of MMP-14 mRNA and protein, proliferation activity, scratch healing rate and invasive cell number of MCF-7 cells in the miR-584-5p mimic+MMP-14 group were higher or morer than those in the miR-584-5p mimic group (P<0.05). The results of double luciferase reporter gene test showed that miR-584-5p could targeted action on the MMP-14 promoter region. Conclusions MiR-584-5p can targetable regulate the expression of MMP-14. Overexpression of miR-584-5p inhibits the proliferation, migration and invasion of breast cancer cells by down-regulating MMP-14.
ObjectiveTo understand the clinical value of centromere proteins (CENPs) in hepatocellular carcinoma and their influence on the malignant biological behavior of hepatocellular carcinoma, and to provide theoretical references for related research in this field. MethodDomestic and international databases were searched for relevant literatures on the study of CENPs in hepatocellular carcinoma in recent years to be analyzed and reviewed. ResultsA total of 11 CENPs closely related to hepatocellular carcinoma had been summarized, which were differentially expressed in hepatocellular carcinoma and correlated with prognosis. CENPs might regulate various malignant biological behaviors such as hepatocellular carcinoma proliferation, metastasis, apoptosis, and resistance to radiotherapy and thus participate in the development of hepatocellular carcinoma via multiple mechanisms. The roles and mechanisms of some CENPs in hepatocellular carcinoma remained unclear. ConclusionsCENPs play an essential role in the diagnosis, treatment, and prognosis of hepatocellular carcinoma. They are involved in multiple malignant biological behaviors of hepatocellular carcinoma and are expected to be potential therapeutic targets for hepatocellular carcinoma. However, their roles and mechanisms in hepatocellular carcinoma remain to be investigated.