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Growth of K562 cells and the expression of CyclinD1 gene and bcr abl fusion gene effected by Genistein

Wei Wang

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Abstract

AIM To investigate the mechanism of how Genistein restrains the growth of K562 cells, and its effect on the expression of CyclinD1 gene and bcr abl fusion gene. METHODS Genistein was incubated with K562 cells, the mRNA of CyclinD1 gene and bcr abl fusion gene were examined by RT PCR and the expression of CDK4 protein, cell cycle and apoptosis were examined by immunofluorescence, flow cytometry and electron microscope at the same time. RESULTS The expression of CyclinD1 gene and bcr abl fusion gene' mRNA was positive in K562 cells. After K562 cells was incubated with Genistein, the expression of bcr abl fusion gene' mRNA and CDK4 protein were negative, mRNA of CyclinD1 gene decreased. And the cell was blocked in G2/M phase. Using electron microscope we could observe the cell's apoptosis. CONCLUSION CyclinD1gene and bcr abl fusion gene are highly expressed in K562 cells. The growth of K562 cells could be restrained by using Genistein, which induces K562 cell's apoptosis, repress the expression of bcr abl fusion gene, and makes CyclinD1 and CDK4 protein decrease. This illuminates that CyclinD1 gene, CDK4 protein and bcr abl fusion gene may have relation to the pathogenesis of chronic myelogenous leukemia (CML).

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AIM To investigate the mechanism of how Genistein restrains the growth of K562 cells, and its effect on the expression of CyclinD1 gene and bcr abl fusion gene. METHODS Genistein was incubated with K562 cells, the mRNA of CyclinD1 gene and bcr abl fusion gene were examined by RT PCR and the expression of CDK4 protein, cell cycle and apoptosis were examined by immunofluorescence, flow cytometry and electron microscope at the same time. RESULTS The expression of CyclinD1 gene and bcr abl fusion gene' mRNA was positive in K562 cells. After K562 cells was incubated with Genistein, the expression of bcr abl fusion gene' mRNA and CDK4 protein were negative, mRNA of CyclinD1 gene decreased. And the cell was blocked in G2/M phase. Using electron microscope we could observe the cell's apoptosis. CONCLUSION CyclinD1gene and bcr abl fusion gene are highly expressed in K562 cells. The growth of K562 cells could be restrained by using Genistein, which induces K562 cell's apoptosis, repress the expression of bcr abl fusion gene, and makes CyclinD1 and CDK4 protein decrease. This illuminates that CyclinD1 gene, CDK4 protein and bcr abl fusion gene may have relation to the pathogenesis of chronic myelogenous leukemia (CML).

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Available abstract

AIM To investigate the mechanism of how Genistein restrains the growth of K562 cells, and its effect on the expression of CyclinD1 gene and bcr abl fusion gene. METHODS Genistein was incubated with K562 cells, the mRNA of CyclinD1 gene and bcr abl fusion gene were examined by RT PCR and the expression of CDK4 protein, cell cycle and apoptosis were examined by immunofluorescence, flow cytometry and electron microscope at the same time. RESULTS The expression of CyclinD1 gene and bcr abl fusion gene' mRNA was positive in K562 cells. After K562 cells was incubated with Genistein, the expression of bcr abl fusion gene' mRNA and CDK4 protein were negative, mRNA of CyclinD1 gene decreased. And the cell was blocked in G2/M phase. Using electron microscope we could observe the cell's apoptosis. CONCLUSION CyclinD1gene and bcr abl fusion gene are highly expressed in K562 cells. The growth of K562 cells could be restrained by using Genistein, which induces K562 cell's apoptosis, repress the expression of bcr abl fusion gene, and makes CyclinD1 and CDK4 protein decrease. This illuminates that CyclinD1 gene, CDK4 protein and bcr abl fusion gene may have relation to the pathogenesis of chronic myelogenous leukemia (CML).

Key concepts: K562 cells, Fusion gene, ABL, Fusion protein, Molecular biology, Chronic myelogenous leukemia, Biology, Gene expression

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Growth of K562 cells and the expression of CyclinD1 gene and bcr abl fusion gene effected by Genistein — Research Paper | ScholarLens