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Hossein-Tehrani, Mohammadjavad, Abbasalipourkabir, Roghayeh, Ziamajidi, Nasrin. (1403). The role of miR-133a in silibinin-mediated inhibition of the PI3K/AKT/mTOR pathway in MCF-7 breast carcinoma cells. , 13(2), 73-83. doi: 10.22099/mbrc.2024.48818.1903
Mohammadjavad Hossein-Tehrani; Roghayeh Abbasalipourkabir; Nasrin Ziamajidi. "The role of miR-133a in silibinin-mediated inhibition of the PI3K/AKT/mTOR pathway in MCF-7 breast carcinoma cells". , 13, 2, 1403, 73-83. doi: 10.22099/mbrc.2024.48818.1903
Hossein-Tehrani, Mohammadjavad, Abbasalipourkabir, Roghayeh, Ziamajidi, Nasrin. (1403). 'The role of miR-133a in silibinin-mediated inhibition of the PI3K/AKT/mTOR pathway in MCF-7 breast carcinoma cells', , 13(2), pp. 73-83. doi: 10.22099/mbrc.2024.48818.1903
Hossein-Tehrani, Mohammadjavad, Abbasalipourkabir, Roghayeh, Ziamajidi, Nasrin. The role of miR-133a in silibinin-mediated inhibition of the PI3K/AKT/mTOR pathway in MCF-7 breast carcinoma cells. , 1403; 13(2): 73-83. doi: 10.22099/mbrc.2024.48818.1903

The role of miR-133a in silibinin-mediated inhibition of the PI3K/AKT/mTOR pathway in MCF-7 breast carcinoma cells

Molecular Biology Research Communications
دوره 13، شماره 2، 2024، صفحه 73-83    اصل مقاله (776.78 K)
نوع مقاله: Original article
شناسه دیجیتال (DOI): 10.22099/mbrc.2024.48818.1903
نویسندگان
Mohammadjavad Hossein-Tehrani1؛ Roghayeh Abbasalipourkabir1؛ Nasrin Ziamajidi* 1، 2
1Department of Clinical Biochemistry, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
2Molecular Medicine Research Center, Hamadan University of Medical Science, Hamadan, Iran
چکیده
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 IC50 value, determined at 370 μM after 48 hours, was established. qRT-PCR analysis at this IC50 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.
کلیدواژه‌ها
Breast neoplasm؛ Silybin؛ miR-133a؛ EGFR؛ PI3K
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