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Cell Journal، جلد ۱۸، شماره ۱، صفحات ۷-۱۲
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عنوان انگلیسی Hsa-miR-590-5p Interaction with SMAD3 Transcript Supports Its Regulatory Effect on The TGFβ Signaling Pathway
چکیده انگلیسی مقاله Objective: SMAD proteins are the core players of the transforming growth factor-beta (TGFβ) signaling pathway, a pathway which is involved in cell proliferation, differentiation and migration. On the other hand, hsa-miRNA-590-5p (miR-590-5p) is known to have a negative regulatory effect on TGFβ signaling pathway receptors. Since, RNAhybrid analysis suggested SMAD3 as a bona fide target gene for miR-590, we intended to investigate the effect of miR-590-5p on SMAD3 transcription. Materials and methods: In this experimental study, miR-590-5p was overexpressed in different cell lines and its increased expression was detected through quantitative reverse transcription-polymerase chain reaction (RT-qPCR). Western blot analysis was then used to investigate the effect of miR-590-5p overexpression on SMAD3 protein level. Next, the direct interaction of miR-590-5p with the 3´-UTR sequence of SMAD3 transcript was investigated using the dual luciferase assay. Finally, flow cytometery was used to investigate the effect of miR-590-5p overexpression on cell cycle progression in HeLa and SW480 cell lines. Results: miR-590-5p was overexpressed in the SW480 cell line and its overexpression resulted in significant reduction of the SMAD3 protein level. Consistently, direct interaction of miR-590-5p with 3´-UTR sequence of SMAD3 was detected. Finally, miR-590-5p overexpression did not show a significant effect on cell cycle progression of Hela and SW480 cell lines. Conclusion: Consistent with previous reports about the negative regulatory effect of miR-590 on TGFβ receptors, our data suggest that miR-590-5p also attenuates the TGFβ signaling pathway through down-regulation of SMAD3.
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نویسندگان مقاله میثم جعفرزاده | meisam jafarzadeh


بهرام m سلطانی | bahram m soltani


نشانی اینترنتی http://celljournal.org/journal/article/abstract/3981
فایل مقاله اشکال در دسترسی به فایل - ./files/site1/rds_journals/16/article-16-367098.pdf
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