ABSTRACT
MicroRNAs(miRNA)are a kind of small non -conding RNA,which negative regulate target genes expression at post -transcription level by binding 3'-untraslation region(3'UTR).Dysregulation of miRNA pro-files relate to cancer,immune disorders,cardiovascular disease,neurodegenerative diseases and metabolic diseases. miR -221 /222 are two similary miRNAs,which share the same promoter and have the same seed sequence.miR -221 /222 usually target to same target genes and co -regulate same processes and act as onco -miRNA roles.Howev-er,miR -221 /222 maybe act as suppressor in cancer which maybe dependent particular context.The roles of miR -221 /222 are reviewed in this article,will provide a comprehensive vision for comprehending the biological process of miR -221 /222 in carcinoma.
ABSTRACT
Objective To investigate the expression of DRAM in breast cancer cell line MCF-7 in radiation-induced autophagy. Methods GFP-LC3 transfection method was used to observe autophagy bubble.Real time-PCR was used to detect DRAM and MAPLC3 from transcriptional and translational level,respectively. The silencing vector from gene engineering was introduced by calcium phosphate transfection.Results Compared with the control group,GFP-LC3 increased significantly after 8 Gy irradiation by immunofluorescent assay,and the level of MAP-LC3 expression was higher than control group after 8 Gy irradiation by Western blot ( F =5.38,8.72,10.63,15.23,20.78 and 55.23,P < 0.05 ).DRAM protein expression increased significantly at 2 h in the 8 Gy time-dose study,up to maximum at the 32 h( F =116.34,P < 0.05 ).In DRAM model,the expression of LC3 and DRAM decreased significantly (F =20.36 and 40.35,P < 0.05 ) and DRAM expression increased 8 Gy post-irradiation,but still lower than that in 8 Gy irradiation wild-type group.The LC3 expression also decreasaed 8 Gy post-irradiation(F =50.34,P < 0.05 ).Conclusions DRAM plays an important role in irradiation-induced autophagy in breast cancer cell.DRAM might participate in the process and serve as a theoretical target for clinical treatment of breast cancer.
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Objective To explore the roles of p53 in ionizing radiation induced MCF-7 cell cycle uncoupling. Methods The p53 knock-down models was established in MCF-7 with retrovirus packaged particles from 293T cells through calcium acid phosphate co-precipitation, then Western blot was used to detect the protein expression. Flow cytometry(FCM) was used to analyze the cell cycle uncoupling and polyploid after irradiation. Results Compared with p53+/+ group, the percentages of G0/G1 cells in p53 -/- group decreased, while those of S and G2+M increased (P < 0.01). In polyploidy analysis 2N cells decreased, whereas both 4N and 8N cells =increased (P<0.01). Compared with sham-irradiation, 4 Gy X-ray led to the decrease of G0/G1, S cells, and the increase of G2+M cells. The increase of 2N cells and decrease of 4N and 8N cells were observed in both p53+/+ and p53-/- cells. Compared with p53+/+ +IR group, the decrease of G0/G1 and S cells and the increase of C2 + M cells were significant (P < 0.01) in p53-/-+ IR groups. 2N cells decreased, 4N cells increased, but no changes in 8 N cells occurred. Conclusion Radiation might induce G2 arrest and cycle uncoupling, p53 plays a role in the regulation of G2 arrest, but no role in cycle uncoupling.