Ahmadi, Moosavi, Hosseinpour Feizi,
Volume 13, Issue 3 (9-2010)
Abstract
Background: Recently, reports have been made of the effects of boric acid (BA) on cancer prevention and inhibition of cancer cell proliferation. This study was designed to investigate the effects of this compound on K562 cell line as a model of chronic myeloid leukemia (CML). Materials and Methods: In this experimental trial, K562 cell line was cultured in the presence of 0.75 to 12 mmol concentrations of boric acid for 24, 48, 72, and 96 hour intervals. Anti-proliferative and cytotoxic effects of BA were measured by trypan blue exclusion test and MTT assay, respectively. Flow-cytometery was utilized for evaluating the effects of BA on cell cycle. Wright-giemsa staining was used for determining the effects of BA, and latex phagocytic assay was used for evaluating the phagocytic potential of the differentiated cells. Results: BA induced growth inhibition of K562 cells in a dose and time dependent manner after 96 hours of treatment with 12 mmol BA, cell proliferation of K562 cells was inhibited to about 83% (p<0.001). In addition, BA induced G1 cell cycle arrest in a way that for instance, after 6 days of treatment with 9 mmol BA, 98% of cell populations were at G1 level. Wright-giemsa staining and latex phagocytic assay results confirmed that K562 cells differentiated toward monocyte-macrophage lineage. Conclusion: Noticing the anti-proliferative and differentiating effects of BA, and no evidence of its adverse effects, this compound can be used as alone or in combination with other drugs in CML differentiation therapy.
Zeynab Hosseinpour, Zivar Salehi, Soheila Talesh Sasani, Keyvan Aminian,
Volume 20, Issue 1 (4-2017)
Abstract
Abstract
Background: Ulcerative colitis (UC) is a chronic disease that specifically affects the mucosa of the rectum and colon. The pathogenesis of UC is not well defined, but it is proposed that genetic and environmental factors result in an aberrant immune response to a subset of commensal enteric bacteria.The aim of this study was to investigate whether miR-34b/c rs4938723 T/C polymorphism is associated with UC risk.
Materials and Methods: Blood samples were collected from 50 patients diagnosed with UC and 100 healthy control subjects. Genomic DNA was extracted from peripheral blood. Genetic variation of miR34b/c was determined by tetra-primers ARMS-PCR (amplification refractory mutation system-polymerase chain reaction). All statistical analyses were conducted using the MedCalc version 12.1.
Results: There was a significant difference in genotype and allele distributions between cases and controls. It was observed that the CT heterozygotes had a 2.29-fold increase in risk of UC (OR=2.29, 95%CI=1.08-4.82, p=0.02).
Conclusion: It is suggested that the miR34b/c (rs4938723 T>C) polymorphism may be associated with the risk of UC. However, larger studies with more patients and controls are needed to confirm this result.
