ArticleCell cycle (Georgetown, Tex.)2015
Epithelial morphological reversion drives Profilin-1-induced elevation of p27(kip1) in mesenchymal triple-negative human breast cancer cells through AMP-activated protein kinase activation.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Profilin and Non-Canonical Wnt Signaling: Coordinating Cytoskeletal Dynamics from Development to Disease.Journal of developmental biology · 2025Review
- Increased expression of Profilin potentiates chemotherapeutic agent-mediated tumour regression.British journal of cancer · 2022Article
- Proteomic Characterization of Cytoplasmic Lipid Droplets in Human Metastatic Breast Cancer Cells.Frontiers in oncology · 2021Article
- Profilin: many facets of a small protein.Biophysical reviews · 2020Review
- Profilin-1 mediated cell-cycle arrest: searching for drug targets.Cell cycle (Georgetown, Tex.) · 2015Article
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5 authors at 2 institutions in 1 country.
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Abstract
Profilin-1 (Pfn1) is an important regulator of actin polymerization that is downregulated in human breast cancer. Previous studies have shown Pfn1 has a tumor-suppressive effect on mesenchymal-like triple-negative breast cancer cells, and Pfn1-induced growth suppression is partly mediated by upregulation of cell-cycle inhibitor p27(kip1) (p27). In this study, we demonstrate that Pfn1 overexpression leads to accumulation of p27 through promoting AMPK activation and AMPK-dependent phosphorylation of p27 on T198 residue, a post-translational modification that leads to increased protein stabilization of p27. This pathway is mediated by Pfn1-induced epithelial morphological reversion of mesenchymal breast cancer through cadherin-mediated restoration of adherens junctions. These findings not only elucidate a potential mechanism of how Pfn1 may inhibit proliferation of mesenchymal breast cancer cells, but also highlight a novel pathway of cadherin-mediated p27 induction and therefore cell-cycle control in cells.
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