ArticleCureus2025
Natural and Synthetic Progestins Increase Transcriptional Expression of primiR-190 and primiR-199 in T47D Breast Cancer Cells: A Preliminary Study.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The diagnostic value and molecular mechanism of miR-199a-5p in recurrent spontaneous abortion.Journal of assisted reproduction and genetics · 2026Article
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3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background Previous studies have shown that aberrant expression of different microRNAs potentially contributes to carcinogenesis, growth, and metastasis of several human cancers. Given that progestins have been reported to alter the expression of microRNAs in various human cancers, we hypothesized that progestins potentially influence the growth of hormone-responsive breast cancer through mechanisms involving the regulation of miRNAs functioning either as tumor suppressors or oncogenes. Using computer-based analysis, we identified two microRNAs that we investigated in this study, namely miR-190 and miR-199. Our main objective in this preliminary study was to determine the effect of different progestins on the expression of these two microRNAs in breast cancer cells. Methods Progesterone receptor (PR)-positive cell line, T47D breast cancer cells were exposed to progesterone and three different synthetic progestins for 24 hours, after which RNA was extracted and real-time polymerase chain reaction (PCR) was used to determine the expression of primiR-190 and primiR-199. For comparison, progestin effects were also tested in T47Dco-Y, a PR-negative cell line. Results Our results showed exposing T47D cells to both progesterone and synthetic progestins increased the transcriptional expression of primiR-190 and primiR-199a1 by as high as four to seven fold (P<0.0001). RU-486, a progesterone receptor antagonist, suppressed progestin induction of both primiR-190 and primiR-199a1. Progestin-induced effects were not observed in a PR-negative subline of T47D cells (P>0.05), further confirming the involvement of progesterone receptor-dependent pathways. Additionally, 17β estradiol and dimethyl sulfoxide did not alter the expression of both primiR-190 and primiR-199a1. Conclusion Different progestins increase transcriptional expression of both primiR-190 and primiR-199a-1 through progesterone receptor (PR)-dependent mechanisms. Both primiR-190 and primiR-199a1 can potentially be useful as biomarkers for PR-positive breast cancer.
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