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JCR 2016
جستجوی مقالات
چهارشنبه 26 آذر 1404
Molecular Biology Research Communications
، جلد ۱۳، شماره ۲، صفحات ۷۳-۸۳
عنوان فارسی
چکیده فارسی مقاله
کلیدواژههای فارسی مقاله
عنوان انگلیسی
The role of miR-133a in silibinin-mediated inhibition of the PI3K/AKT/mTOR pathway in MCF-7 breast carcinoma cells
چکیده انگلیسی مقاله
Breast cancer is particularly severe in women. Research highlights the crucial role of miRNAs in key cellular processes, showcasing their intricate interactions with the oncogenic PI3K/AKT/mTOR (PAM) signaling pathway and underscoring their significant role as tumor suppressors. The effect of silibinin on cell growth and survival was evaluated using an MTT assay. Bioinformatics analysis identified putative miR-133a targets inside the PAM pathway. After incubating MCF-7 cells with silibinin, we measured miR-133a,
EGFR
,
PI3K
,
AKT
,
PTEN
, and
mTOR
expression levels using qRT-PCR. Furthermore, protein expression levels of mTOR were assessed using Western blotting. The MTT experiment displayed that silibinin effectively inhibits MCF-7 cell proliferation in a time- and dose-dependent manner. Silibinin's IC
50
value, determined at 370 μM after 48 hours, was established. qRT-PCR analysis at this IC
50
concentration highlighted reduced expression of
EGFR
,
PI3K
,
AKT
,
PTEN
, and
mTOR
mRNAs, alongside increased miR-133a expression. Notably, miR-133a exhibited a negative correlation with both
EGFR
and
PIK3C2A
expression. Furthermore, western blotting confirmed silibinin's capacity to diminish p-mTOR protein levels, the ultimate element of the PAM signaling pathway. The findings enhance comprehension of silibinin's impact on PAM signaling and miR-133a expression, offering promise for targeted therapies in disrupting oncogenic pathways in MCF-7 breast cancer cells. This insight could advance breast cancer treatment strategies.
کلیدواژههای انگلیسی مقاله
Breast neoplasm, Silybin, miR-133a, EGFR, PI3K
نویسندگان مقاله
Mohammadjavad Hossein-Tehrani |
Department of Clinical Biochemistry, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
Roghayeh Abbasalipourkabir |
Department of Clinical Biochemistry, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
Nasrin Ziamajidi |
Department of Clinical Biochemistry, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
نشانی اینترنتی
https://mbrc.shirazu.ac.ir/article_7378_695d98f25b3db0a801be9a7bbbaf5a90.pdf
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