RESUMO
<p><b>BACKGROUND</b>Id3 plays a key role in the progression of breast cancer. Previously, four and a half LIM protein (FHL2) was identified as a repressor of Id family proteins by interacting with them. This study aimed to investigate the effects of FHL2 on the transcriptional regulation and oncogenic activities of Id3 in human breast cancer cells.</p><p><b>METHODS</b>Cell transfection was performed with SuperFect reagent. Stable transfectants that overexpressed Id3 were obtained by selection on G418. The level of Id3 protein was determined by Western blotting analysis. Dual luciferase assays were used to measure the effect of Id3 and FHL2 on E47-mediated transcriptional activity in MCF-7 human breast cancer cells. The MTT assay was used to measure cell proliferation. The transwell assay was used to measure the invasive capacity of MCF-7 cancer cells.</p><p><b>RESULTS</b>Id3 markedly repressed transcription mediated by the basic helix-loop-helix (bHLH) factor E47 in MCF-7 cells. This Id3-mediated repression was effectively antagonized by FHL2. Overexpression of Id3 markedly promoted the proliferation and invasive capacity of MCF-7 cells; however, these effects were significantly suppressed by the overexpression of FHL2.</p><p><b>CONCLUSIONS</b>FHL2 can inhibit the proliferation and invasive growth of human breast cancer cells by repressing the functional activity of Id3. The functional roles of FHL2-Id3 signaling in the development of human breast cancer need further research.</p>
Assuntos
Humanos , Western Blotting , Neoplasias da Mama , Genética , Metabolismo , Linhagem Celular Tumoral , Proliferação de Células , Proteínas Inibidoras de Diferenciação , Genética , Metabolismo , Proteínas com Homeodomínio LIM , Genética , Metabolismo , Células MCF-7 , Proteínas Musculares , Genética , Metabolismo , Proteínas de Neoplasias , Genética , Metabolismo , Fator 3 de Transcrição , Genética , Metabolismo , Fatores de Transcrição , Genética , MetabolismoRESUMO
<p><b>OBJECTIVE</b>To investigate the protective effect of leptin against cerebral ischemia/reperfusion injury in mice.</p><p><b>METHODS</b>Mouse models of transient focal cerebral ischemia were established by occlusion of the right middle cerebral artery for 2 h followed by 24 h reperfusion. The infarct volume and neurological deficit scores following leptin treatment were determined using TTC staining and the Longa's score, respectively, to evaluate the protective effect of leptin against ischemic cerebral injury. The levels of lactate dehydrogenase (LDH), malondialdehyde (MDA) and nitric oxide (NO) in the brain tissue were measured by colorimetry. The histopathological changes in the brain were observed with HE staining, and the expression of glial fibrillary acidicprotein (GFAP) was detected by immunohistochemistry.</p><p><b>RESULTS</b>Leptin treatment markedly reduced cerebral infarct volume and neurological deficits induced by transient ischemia. The LDH, MDA and NO levels in the brain tissues were significantly decreased after leptin treatment, which also alleviated the histopathological injury, maintained the normal morphology of the astrocytes and increased the expression of GFAP.</p><p><b>CONCLUSION</b>Leptin produces obvious protective effect against cerebral ischemia/reperfusion injury by inhibiting lipid peroxidation, stabilizing the internal environment and adjusting the activity of the astrocytes.</p>