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1.
Journal of Experimental Hematology ; (6): 1780-1784, 2021.
Artículo en Chino | WPRIM | ID: wpr-922334

RESUMEN

OBJECTIVE@#To investigate the effect of RITA on TP53 mutant human mantle cell lymphoma (MCL) cell line Mino and its possible mechanism.@*METHODS@#Mino cells were cultured in RPMI-1640 and treated with RITA at a concentration of 0-16 μmol/L for 24,48,72 hours. Cell viability was assessed by CCK-8 assay. The cells were treated by RITA (0-8 μmol/L) for 48 h, the cell apoptosis induced by RITA was detected by annexin V/PI flow cytometry. Western blot was performed to evaluate the expression of protein BCL-2, Caspase-3, Cleaved Caspase-3, PARP, MDM2, and P53 in Mino cells.@*RESULTS@#After treatment with 0.5, 1, 2, 4, 8, and 16 μmol/L RITA for 48 h, the proliferation inhibition rate of Mino cells was (1.2±5.6)%, (14.9±4.9)%, (41.7±5.0)%, (61.8±2.4)%, (70.2±2.8)%, and (70.8±2.4)%, respectively. RITA could inhibit the proliferation of Mino cells significantly, and statistical analysis showed that the inhibition rate was increased with the increasing of RITA concentration (r=0.767). After the cells were treated by 4 μmol/L RITA for 24, 48, and 72 h, the proliferation inhibition rate was (25.2±3.8)%, (61.8±2.4)%, and (87.0±0.7)%, respectively. Satistical analysis showed that the inhibition rate was also increased with the increasing of treatment time (r=0.978). The apoptosis rate of Mino cells treated by 0, 2, 4, and 8 μmol/L RITA for 48 h was (5.4±0.4)%, (15.3±0.6)%, (38.7±1.7)%, and (50.8±1.1)%, respectively, and it showed dose-dependent manner (r=0.961). Western blot showed that with the increasing of RITA concentration, the BCL-2 protein expression was decreased in a dose-dependent manner (r=0.932), moreover, PARP cleavage and Caspase-3 activation were found, while the protein expression of MDM2 and P53 showed no change.@*CONCLUSION@#RITA can inhibit the proliferation and induce the apoptosis of Mino cells significantly. The mechanism may be dependent on the Caspase pathway, but independent on the P53 pathway.


Asunto(s)
Humanos , Apoptosis , Línea Celular Tumoral , Supervivencia Celular , Furanos , Linfoma de Células del Manto , Mutación , Proteína p53 Supresora de Tumor
2.
Artículo en Chino | WPRIM | ID: wpr-360124

RESUMEN

<p><b>OBJECTIVE</b>To investigate the effect of bortezomib in inducing apoptosis in imatinib-resistant K562 (K562R) cells and its possible mechanism.</p><p><b>METHODS</b>K562 cells were cultured in gradient concentrations of imatinib for several months to generate imatinib-resistant K562 cells. The viability of K562R cells treated with bortezomib was measured using CCK-8 cell proliferation assay, and the cell apoptosis was analyzed by flow cytometry with annexin V/PI dual staining. Western blotting was used to detect the protein expressions of Mcl-1,Bcl-2 and Bcr/Abl.</p><p><b>RESULTS</b>K562R cell line was successfully established, which showed 31.8 folds of imatinib resistance compared with the na?ve cells. Bortezomib treatment produced dose- and time-dependent inhibitory effect on the proliferation of both K562 cells and K562R cells and dose-dependently induced apoptosis in K562R cells. Combination of bortezomib with imatinib significantly enhanced the apoptosis of the cells. Western blotting showed that bortezomib treatment dose-dependently decreased the protein levels of both Mcl-1and Bcr/Abl in K562R cells without affecting bcl-2 protein expression.</p><p><b>CONCLUSION</b>Bortezomib can inhibit the proliferation of K562R cells and induce cell apoptosis possibly by down-regulating Mcl-1 and Bcr/Abl expression and enhancing Mcl-1 cleavage.</p>

3.
Artículo en Chino | WPRIM | ID: wpr-360087

RESUMEN

<p><b>OBJECTIVE</b>To investigate miR-181a function and regulation mechanism by identifying miR-181a target genes in acute myeloid leukemia (AML).</p><p><b>METHODS</b>The HL-60 cells of human AML was transfected by small molecular analog miR-181a, the cell proliferation was detected by CCK-8 method after electroporation in HL-60 cell lines. Target genes of miR-181a were predicted and analyzed by the bioinformatics software and database. Target genes were confirmed by HL-60 cell line and the patient leukemia cells.</p><p><b>RESULTS</b>Overexpressed miR-181a in HL-60 cell line significantly enhanced cell proliferation compared with that in control (P < 0.05). Dual luciferase reporter gene assay showed that miR-181a significantly suppressed the reporter gene activity containing ATM 3'-UTR by about 56.8% (P < 0.05), but it didn't suppress the reporter gene activity containing 3'-UTR ATM mutation. Western blot showed that miR-181a significantly downregulated the expression of ATM in human leukemia cells. It is also found that miR-181a was significantly increased in AML, which showed a negative correlation with ATM expression.</p><p><b>CONCLUSION</b>miR-181a promotes cell proliferation in AML by regulating the tumor suppressor ATM, thus it plays the role as oncogene in pathogenesis of AML.</p>


Asunto(s)
Humanos , Proteínas de la Ataxia Telangiectasia Mutada , Metabolismo , Proliferación Celular , Regulación hacia Abajo , Células HL-60 , Leucemia Mieloide Aguda , Metabolismo , Patología , MicroARNs , Genética , Metabolismo , Transfección
4.
Artículo en Chino | WPRIM | ID: wpr-235156

RESUMEN

<p><b>OBJECTIVE</b>To analyze the molecular pathogenesis of protein S deficiency in an adolescent case of recurrent deep vein thrombosis (DVT).</p><p><b>METHODS</b>Blood samples from the patient and his family members were collected for detection of the coagulation parameters by one-step clotting method, and the protein S (PS) and protein C activities were measured by a chromogenic assay. Enzyme-linked immunosorbent assay was employed for detecting the levels of free PS antigen. All the exons and exon-intron boundaries of the patients PS gene were amplified using PCR and analyzed by direct sequencing.</p><p><b>RESULTS</b>As carriers of hereditary PS deficiency, both the patient and his father showed a heterozygous C82792T point mutation in the 10th exon of their PS gene which resulted in the substitution of arginine314 by cysteine in the polypeptide chain of PS protein.</p><p><b>CONCLUSION</b>Recurrence of DVT in this patient is the result of hereditary PS deficiency caused by a novel heterozygous missense mutation in the PS gene.</p>


Asunto(s)
Adolescente , Humanos , Masculino , Sustitución de Aminoácidos , China , Heterocigoto , Mutación Missense , Linaje , Mutación Puntual , Proteína S , Genética , Deficiencia de Proteína S , Genética , Recurrencia , Trombosis de la Vena , Genética
5.
Artículo en Chino | WPRIM | ID: wpr-355010

RESUMEN

<p><b>OBJECTIVE</b>To study the relationship between the donor and recipient serum interleukin 2 (IL-2) and tumor necrosis factor alpha (TNF-alpha) levels and the occurrence of acute graft-versus-host disease (aGVHD) following hematopoietic stem cell transplantation.</p><p><b>METHODS</b>Twenty-two leukemic patients undergoing allo-hematopoietic stem cells transplantation and their donors were examined for serum levels of IL-2 and TNF-alpha using ELISA during conditioning and after the transplantation. IL-2 and TNF-alpha levels were also detected in the donors during mobilization to analyze the relationship between the cytokines and aGVHD.</p><p><b>RESULTS</b>Five recipients showed no aGVHD, 10 developed grade I aGVHD, and 7 developed grade II-IV aGVHD. The serum levels of IL-2 and TNF-alpha after conditioning and post-transplantation were significantly higher in the recipients with grade II-IV aGVHD than in those with grade 0-I aGVHD, but no difference was found before the pre-conditioning. The serum IL-2 levels in the mobilized donors for the recipients with grade II-IV aGVHD were significantly higher than that in donors for recipients with grade 0-I aGVHD, whereas the levels of TNF-alpha showed no such a difference.</p><p><b>CONCLUSION</b>Serum IL-2 and TNF-alpha levels in the leukemic patients after conditioning and post-transplantation, and the donor serum IL-2 level after mobilization may be correlative to the severity of aGVHD and can be used as indicators for predicting the severity of aGVHD after the transplantation.</p>


Asunto(s)
Adolescente , Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Adulto Joven , Enfermedad Injerto contra Huésped , Diagnóstico , Trasplante de Células Madre Hematopoyéticas , Interleucina-2 , Sangre , Leucemia , Terapéutica , Donantes de Tejidos , Factor de Necrosis Tumoral alfa , Sangre
6.
Chinese Journal of Hematology ; (12): 587-589, 2007.
Artículo en Chino | WPRIM | ID: wpr-262980

RESUMEN

<p><b>OBJECTIVE</b>To identify the antithrombin (AT) phenotype and gene mutation of a kindred with hereditary antithrombin deficiency.</p><p><b>METHODS</b>Plasma AT activity and AT antigen level of the propositus and his kindred members were determined with chromogenic substrate method and immunoassay, respectively. All the seven exons and intron-exon boundaries of antithrombin gene were analyzed by PCR and direct sequencing of amplified PCR products from the propositus.</p><p><b>RESULTS</b>The propositus AT antigen level was normal but his AT activity was only 65% of normal value suggesting that he had type II AT deficiency. A heterozygous G13830A mutation in exon 6 resulting in Arg393His missense mutation in his AT polypeptide was identified in the propositus. The same phenotype and gene mutation were found in other 3 kindred members.</p><p><b>CONCLUSION</b>The type II AT deficiency found in this kindred is caused by heterozygous G13830A mutation in AT gene.</p>


Asunto(s)
Adulto , Humanos , Masculino , Antitrombina III , Genética , Metabolismo , Deficiencia de Antitrombina III , Genética , Heterocigoto , Mutación , Linaje
7.
Artículo en Chino | WPRIM | ID: wpr-278871

RESUMEN

The aim was to study the morphological, histochemical and immunological characteristics of less-differentiated acute myeloid leukemic cells, and their diagnostic significance. Wright-Giemsa and histochemical staining were used to stain bone marrow smears from 2 case of AML-Mo. Immunological phenotypes were determined with flow cytometry. The results showed that myeloperoxidase stainings of both cases were negative, PAS was positive with fine particles, CD33/CD13 were positive, CD2/CD3/CD10/CD19/CD22 were negative. It is concluded that morphology, histochemistry and immunological phenotype on bone marrow smears are the main diagnostic basis for AML-Mo. The use of multiple monoclonal antibodies for staining may improve the accuracy.


Asunto(s)
Femenino , Humanos , Persona de Mediana Edad , Diferenciación Celular , Leucemia Mieloide Aguda , Clasificación , Alergia e Inmunología , Patología
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