Investigation of the functions of candidate miRNAs in camptothecin-induced apoptosis in human cells için kapak resmi
Investigation of the functions of candidate miRNAs in camptothecin-induced apoptosis in human cells
Başlık:
Investigation of the functions of candidate miRNAs in camptothecin-induced apoptosis in human cells
Yazar:
Demir, Şeyda.
Yazar Ek Girişi:
Yayın Bilgileri:
[s.l.]: [s.n.], 2012.
Fiziksel Tanımlama:
ix, 22 leaves. : ill. + 1 computer laser optical disc.
Özet:
MicroRNAs are non-coding 19-25nt long, small RNAs that regulate expression of about 30% of human genes by inhibiting mRNA translation or inducing its degradation. MicroRNAs play important role in cell growth, differentiation, apoptosis. miRNAs regulate apoptosis by targeting genes involved in apoptotic pathway as a pro or anti-apoptotic genes. This study has aimed to identify whether candidate miRNAs ( miR-17* and miR-425) have a regulatory role in camptothecin induced apoptosis or not in Human cells and Hela cells that derived from cervical cancer were used as a model cell line. These candidates were selected based on deep sequencing data that showed some miRNAs differentially expressed after camptothecin treatment as compared with non-treated control group. To show candidate miRNAs whether have a role or not in regulation of camptothecin induced apoptosis, first Hela cells were transfected with candidate miRNAs then candidate miRNA over-expressed cells were treated with camptothecin eventually level of apoptosis was measured by flow cytometry and the results were evaluated by comparing miRNA over-expressed cell group with un-transfected control group. Active caspase-3 level also was measured by using flow cytometry and the data showed miR-17* and miR-425 function as pro-apoptotic regulator in camptothecin induced apoptosis in Hela cells.
Yazar Ek Girişi:
Tek Biçim Eser Adı:
Thesis (Master)--İzmir Institute of Technology: Molecular Biology and Genetics.

İzmir Institute of Technology: Molecular Biology and Genetics.
Elektronik Erişim:
Access to Electronic Versiyon.
Ayırtma: Copies: