ABSTRACT
To explore the clinical application value of 3-dimensional and multiplane reconstruction with MSCT in diagnosing costal cartilage trauma. Totally 19 cases with costal cartilage trauma underwent MSCT 5 mm scanning and 0.625 mm reconstruction, and then went through three-dimensional and multiplane reconstruction. The ac-quired data were transmitted to the computer workstation through the network, and then three-reconstruction was per-formed with the software on AW4.3 platform. There were all 32 costal cartilage fractures in the 19 patients in-volving 15 cases with rib fracture, which included 2 cases and 3 fractures at the chondrosternal junction, 13 cases and 25 fractures in the middle of the costal cartilage, 4 cases and 4 fractures at the junction between costal cartilage and rib. Three-dimensional reconstruction with spiral CT could display clearly the location and number of costal cartilage frac-tures. Three-dimensional and multiplane reconstruction shows clearly the fracture and displacement of the costal cartilage, and the combination of MRP, MIR and VR may contribute to the diagnosis and clinical planning of the costal cartilage fracture.
ABSTRACT
MicroRNAs (miRNAs) are small, non-coding RNAs that function as post-transcriptional regulators of gene expression. The deregulated expression of miRNAs is associated with a variety of diseases, including breast cancer. In the present study, we found that miR-495 was markedly up-regulated in clinical breast cancer samples by quantitative real time-PCR (qRT-PCR). Junctional adhesion molecule A (JAM-A) was predicted to be a potential target of miR-495 by bioinformatics analysis and was subsequently verified by luciferase assay and Western blotting. JAM-A was found to be negatively correlated with the migration of breast cancer cells through loss-of-function and gain-of-function assays, and the inhibition of JAM-A by miR-495 promoted the migration of MCF-7 and MDA-MB-231 cells. Furthermore, overexpression of JAM-A could restore miR-495-induced breast cancer cell migration. Taken together, our findings suggest that miR-495 could facilitate breast cancer progression through the repression of JAM-A, making this miRNA a potential therapeutic target.
Subject(s)
Adult , Aged , Female , Humans , Middle Aged , 3' Untranslated Regions , Genetics , Blotting, Western , Breast Neoplasms , Genetics , Metabolism , Pathology , Cell Adhesion Molecules , Genetics , Metabolism , Cell Line, Tumor , Cell Movement , Genetics , Gene Expression Regulation, Neoplastic , Gene Knockdown Techniques , MCF-7 Cells , MicroRNAs , Genetics , RNA Interference , Receptors, Cell Surface , Genetics , Metabolism , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
Objective Tumor suppressor gene p53 can inhibit tumor cell growth, arrest cell cycle, and promote apoptosis.Howev-er, the effects of p53 on the pathogenesis of breast cancer have not been fully elucidated.The aim of this study was to explore the expression of p53 protein and the correlation with clinical pathologic features in breast cancer.Furthermore, the regulatory effects of 5-aza-2′-deoxycyti-dine on p53 in breast cancer cell line were also studied. Methods The expression of p53 protein in 80 cases of breast cancer and normal and adjacent tissue were determined by the immunohistochemical staining .The expressions of p53 mRNA and p53 protein in breast cancer cell line were determined by RT-PCR and Western blotting. Results The positive rate of p53 in breast cancer (41.25%) was higher than that in the normal and adjacent tissue (22.5%) (P0.05).The low expression of p53 both in mRNA and in protein levels were found in breast cancer cell line of MCF-7.The expres-sion of p53 increased after 5-aza-2′-deoxycytidine administration . Conclusion p53 is highly expressed in breast cancer , which may play an im-portant role in the development and progression of breast cancer. 5-aza-2′-deoxycytidine, up-regulating the p53 expression in breast cancer cell line, which provides the evidents for the development of therapeutic drugs for the patients with low expression of p53 breast cancer.