|
|
|
|
|
| Zhou,L.L.; Dong,J.L.; Huang,G.; Sun,Z.L.; Wu,J.. |
| This study aimed to investigate the function and mechanism of microRNA-143 (miR-143) in the occurrence and development of breast cancer (BC). A total of 30 BC tissues, 30 corresponding noncancerous tissues, and 10 normal control (NC) breast tissues were obtained to detect the levels of miR-143, extracellular signal-regulated kinase 5 (ERK5) and mitogen-activated protein 3 kinase 7 (MAP3K7) using RT-qPCR, western blotting or immunohistochemistry. The correlation of miR-143 with ERK5 or MAP3K7 was evaluated using Pearson correlation analysis. MCF-7 cells were transiently transfected with miR-143 mimic, miR-143 inhibitor, miR-143 mimic/inhibitor + si-ERK5, si-MAP3K7 or si-cyclin D1. Then, cell growth was evaluated by MTT assay and the expressions of... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Extracellular signal-regulated kinase 5; Mitogen-activated protein 3 kinase 7; MiRNA-143; Breast cancer; Cyclin D1. |
| Ano: 2017 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2017000800608 |
| |
|
| |
|
|
| Wenner,C.E.; Yan,S.. |
| TGF-ß1 regulates both cellular growth and phenotypic plasticity important for maintaining a growth advantage and increased invasiveness in progressively malignant cells. Recent studies indicate that TGF-ß-1 stimulates the conversion of epitheliod to fibroblastoid phenotype which presumably leads to the inactivation of growth-inhibitory effects by TGF-ß1 (Portella et al. (1998) Cell Growth and Differentiation, 9: 393-404). Therefore, the investigation of TGF-ß1 signaling that leads to altered growth and migration may provide novel targets for the prevention of increased cell growth and invasion. Although much attention has been paid to TGF-ß1 responses in epithelial cells, the above studies suggest that examination of signal transduction pathways in... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Transforming growth factor; MAP kinase; Cyclin D1. |
| Ano: 1999 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1999000700004 |
| |
|
|
| Fukumasu,H.; Cordeiro,Y.G.; Rochetti,A.L.; Barra,C.N.; Sámora,T.S.; Strefezzi,R.F.; Dagli,M.L.Z.. |
| Nuclear receptor subfamily 1, group I, member 3 (NR1I3) is reported to be a possible novel therapeutic target for some cancers, including lung, brain and hematopoietic tumors. Here, we characterized expression of NR1I3 in a mouse model of lung carcinogenesis induced by 4-(methylnitrosamino)-4-(3-pyridyl)-1-butanone (NNK), the most potent tobacco carcinogen. Lung tumors were collected from mice treated with NNK (400 mg/kg) and euthanized after 52 weeks. Benign and malignant lesions were formalin-fixed and paraffin-embedded for histology and immunohistochemistry, with samples snap-frozen for mRNA analysis. Immunohistochemically, we found that most macrophages and type I and II pneumocytes expressed NR1I3, whereas fibroblasts and endothelial cells were... |
| Tipo: Info:eu-repo/semantics/report |
Palavras-chave: NR1I3; CAR; NNK; Cyclin D1; Lung carcinogenesis. |
| Ano: 2015 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2015000300240 |
| |
|
|
|
