ArticleOncogene2015
Progesterone downregulation of miR-141 contributes to expansion of stem-like breast cancer cells through maintenance of progesterone receptor and Stat5a.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 73 citations in OpenAlex.
- Advances in intratumoral immunotherapy from a neuro-immune-endocrine perspective for breast cancer treatment.Frontiers in oncology · 2026Review
- Recent Advances (2020-2025) in Estrogen and ER-Positive Breast Cancer: Receptor Signaling, Tumor Microenvironment, Endocrine Therapy Resistance and Innovative Treatment Strategies-A Comprehensive Review.Cancer management and research · 2026Review
- Site-specific O-GlcNAcylation of progesterone receptor (PR) supports PR attenuation of interferon stimulated genes (ISGs) and tumor growth in breast cancer.The Journal of biological chemistry · 2024Article
- Progesterone Receptor Signaling Promotes Cancer Associated Fibroblast Mediated Tumorigenicity in ER+ Breast Cancer.Endocrinology · 2024Article
- Dynamic interplay of nuclear receptors in tumor cell plasticity and drug resistance: Shifting gears in malignant transformations and applications in cancer therapeutics.Cancer metastasis reviews · 2024Review
- Screening and validation of novel serum panel of microRNA in stratification of prostate cancer.Prostate international · 2023Article
- Identification of potential microRNA diagnostic panels and uncovering regulatory mechanisms in breast cancer pathogenesis.Scientific reports · 2022Article
- High Levels of Progesterone Receptor B in MCF-7 Cells Enable Radical Anti-Tumoral and Anti-Estrogenic Effect of Progestin.Biomedicines · 2022Article
- Progesterone Receptors Promote Quiescence and Ovarian Cancer Cell Phenotypes via DREAM in p53-Mutant Fallopian Tube Models.The Journal of clinical endocrinology and metabolism · 2021Article
- Expression analysis of progesterone‑regulated miRNAs in cells derived from human glioblastoma.Molecular medicine reports · 2021Article
- Long non-coding RNA NEAT1 transported by extracellular vesicles contributes to breast cancer development by sponging microRNA-141-3p and regulating KLF12.Cell & bioscience · 2021Article
- MicroRNA Regulation of Breast Cancer Stemness.International journal of molecular sciences · 2021Review
- LncRNAs and microRNAs as Essential Regulators of Stemness in Breast Cancer Stem Cells.Biomolecules · 2021Review
- Nanosized Drug Delivery Systems for Breast Cancer Stem Cell Targeting.International journal of nanomedicine · 2021Review
- Potential Diagnostic and Prognostic Utility of miR-141, miR-181b1, and miR-23b in Breast Cancer.International journal of molecular sciences · 2020Article
- Regulation of breast cancer metastasis signaling by miRNAs.Cancer metastasis reviews · 2020Review
- microRNA Expression Profile in Single Hormone Receptor-Positive Breast Cancers is Mainly Dependent on HER2 Status-A Pilot Study.Diagnostics (Basel, Switzerland) · 2020Article
- 90 YEARS OF PROGESTERONE: Progesterone and progesterone receptors in breast cancer: past, present, future.Journal of molecular endocrinology · 2020Review
- Regulatory Mechanism of MicroRNA Expression in Cancer.International journal of molecular sciences · 2020Review
- Influence of MicroRNA-141 on Inhibition of the Proliferation of Bone Marrow Mesenchymal Stem Cells in Steroid-Induced Osteonecrosis via SOX11.Orthopaedic surgery · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Progesterone (P4) has emerged as an important hormone-regulating mammary stem cell (MaSC) populations. In breast cancer, P4 and synthetic analogs increase the number of stem-like cells within luminal estrogen receptor (ER)- and progesterone receptor (PR)-positive breast cancers. These cells gain expression of de-differentiated cell markers CD44 and cytokeratin 5 (CK5), lose luminal markers ER and PR, and are more therapy resistant. We previously described that P4 downregulation of microRNA (miR)-29a contributes to the expansion of CD44(high) and CK5(+) cells. Here we investigated P4 downregulation of miR-141, a member of the miR-200 family of tumor suppressors, in facilitating an increase in stem-like breast cancer cells. miR-141 was the sole member of the miR-200 family P4-downregulated at the mature miRNA level in luminal breast cancer cell lines. Stable inhibition of miR-141 alone increased the CD44(high) population, and potentiated P4-mediated increases in both CD44(high) and CK5(+) cells. Loss of miR-141 enhanced both mammosphere formation and tumor initiation. miR-141 directly targeted both PR and signal transducer and activator of transcription 5A (Stat5a), transcription factors important for MaSC expansion. miR-141 depletion increased PR protein levels, even in cell lines where PR expression is estrogen dependent. Stat5a suppression via small interfering RNA or a small-molecule inhibitor reduced the P4-dependent increase in CK5(+) and CD44(high) cells. These data support a mechanism by which P4-triggered loss of miR-141 facilitates breast cancer cell de-differentiation through deregulation of PR and Stat5a, two transcription factors important for controlling mammary cell fate.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.