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1.
Chinese Journal of Hematology ; (12): 1010-1014, 2013.
Article in Chinese | WPRIM | ID: wpr-295751

ABSTRACT

<p><b>OBJECTIVE</b>To investigate miR- 125b regulation mechanism by identifying miR-125b target genes and its function in acute myeloid leukemia (AML).</p><p><b>METHODS</b>The bioinformatics software and database were applied to predict and analyze target genes of miR-125b. The vector contained the target gene 3'-UTR portion cloned into a luciferase reporter construct. A luciferase reporter assay was performed following co-transfection of small molecular miR-125b mimics and target gene wild-type or mutant plasmid into HEK-293T cells. Further in leukemia cell lines NB4 and HL-60, the protein level of target gene was measured by Western blot after overexpression miR-125b. Finally, the viabilities of NB4 and HL-60 cells were measured by CCK-8 assay at 24 h, 48 h, 72 h, 96 h after electroporation.</p><p><b>RESULTS</b>Bcl-2-antagonist/killer 1 (Bak1), a pro-apoptotic gene, was a target gene of miR-125b by software predicts. Reporter vector containing the 3'-UTR Bak1 wild and mutation sites were co-transfected with small molecule analogues of miR-125b in HEK-293T cells. Dual luciferase reporter gene assay system showed that miR-125b significantly suppresses the reporter gene activity containing Bak1 3'-UTR by about 53.8% (P<0.05), but it didn't suppresses the reporter gene activity containing 3'-UTR Bak1 mutation. Western blot showed that miR-125b mimics significantly down-regulated the expression of Bak1 in human leukemia cell lines NB4 and HL-60. Meanwhile, the growth rate of cells treated with miR-125b obviously increased compared with that in control by CCK-8 test (P<0.05).</p><p><b>CONCLUSION</b>Our findings strongly indicated that BAK1 was a downstream target gene of miR-125b, and miR-125b promoted proliferation in human AML cells at least partially by targeting Bak1, so we speculated that miR-125b as an oncogene could be a potential therapeutic target for treating AML.</p>


Subject(s)
Humans , Cell Line, Tumor , Cell Proliferation , Genetic Vectors , HEK293 Cells , HL-60 Cells , MicroRNAs , Genetics , Transfection , bcl-2 Homologous Antagonist-Killer Protein , Genetics , Metabolism
2.
Chinese Journal of Contemporary Pediatrics ; (12): 311-314, 2006.
Article in Chinese | WPRIM | ID: wpr-262708

ABSTRACT

McCune-Albright syndrome is a rare G proteins alpha disorder. The disorder is characterized by polyostotic fibrous dysplasia, sexual precocity and hyperpigmented macules. It is caused due to mutations in the gene Gsalpha that incodes the alpha subunit of the trimeric guanosine triphate-binding protein. There is no specific treatment for this syndrome. Treatment is generally symptomatic. This paper reported three cases of McCune-Albright syndrome and reviewed the relevant literatures regarding to the pathogenesis, pathological features, diagnosis and treatment. All three cases presented with a characteristic triad: polyostotic fibrous dysplasia, sexual precocity and hyperpigmented macules and were thus definitely diagnosed with McCune-Albright syndrome.


Subject(s)
Child , Child, Preschool , Female , Humans , Diagnosis, Differential , Fibrous Dysplasia, Polyostotic , Diagnosis , Pathology , Therapeutics , Prognosis
3.
Journal of Applied Clinical Pediatrics ; (24)2006.
Article in Chinese | WPRIM | ID: wpr-638951

ABSTRACT

Objective To explore the clinical characteristics and emergency treatment for type 1 diabetes(T1DM) and diabetes ketoacidosis(DKA) in children under 5 years old.Methods Twenty-one children under 5 years old with T1DM with 10 years were retrospecti-vely reviewed.The onset situation,clinical feature and treatment of DKA were analyzed.Results The cases of little children diabetes might not have typical symptoms.The positivity of islet antibody was lower.High morbidity of DKA was found in little children and DKA was often caused by infection.Conclusions Infection may be involved in the onset and progress of childhood T1DM.Emergency treatment for DKA may involve the injection of small dose insulin,correction of the disorder of water and electrolysis and regulation of acid-base.

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