ArticleInternational journal of oncology2025
Progerin regulates actin cytoskeletal remodeling and inhibits EMT and metastasis in triple‑negative breast cancer cells.
Article in International journal of oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- HNMT promotes the motility-associated structures of breast cancer cells through the PI3K/Akt signaling pathway to promote tumor progression.Histology and histopathology · 2026Article
- Exploration of the mechanism of hesperidin inhibition on the proliferation and metastasis of human breast cancer cells.International journal of clinical and experimental pathology · 2026Article
- Hesperidin Inhibits Proliferation and Metastasis of Human Breast Cancer Cells by Suppressing MMP-2/9 Activity and Reversing Epithelial-Mesenchymal Transition.Cancer informatics · 2026Article
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5 authors.
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Abstract
Triple‑negative breast cancer (TNBC) is a subtype of breast cancer, known for its poor prognosis due to its high invasiveness, strong metastatic tendencies and propensity for recurrence. Epithelial to mesenchymal transition (EMT) is a crucial process in tumor invasion and metastasis and in the formation of cancer‑initiating cells. Hutchinson‑Gilford progeria is a rare condition characterized by accelerated aging, caused by a mutated form of lamin A, known as progerin. The present study aimed to investigate the effect of progerin overexpression on TNBC and uncover its underlying mechanisms of action. Therefore, cell senescence was assessed using senescence‑associated β‑galactosidase staining, while cell proliferation was measured by colony formation, Cell Counting Kit‑8 and EdU assays. Additionally, cell metastasis was evaluated using wound‑healing, Transwell and cell adhesion assays. Immunofluorescence staining was carried out to observe actin cytoskeleton and nuclear morphology. The results showed that progerin markedly suppressed the colony formation, migration, invasion and adhesion abilities of BT‑549 and MDA‑MB‑231 TNBC cell lines, without affecting cell senescence or proliferation. In addition, progerin overexpression altered nuclear morphology and actin cytoskeleton organization in TNBC cells. Furthermore, the expression levels of the mesenchymal markers, N‑cadherin, vimentin, Snail and Slug, were reduced, while those of the epithelial marker, E‑cadherin, were enhanced in TNBC cells. Overall, the results of the present study suggested that progerin overexpression could inhibit TNBC cell metastasis, probably via actin cytoskeleton remodeling and regulate the expression levels of the cytoskeletal‑related proteins, anillin and β‑catenin, and those of the EMT‑related ones. The aforementioned findings could provide novel insights into the identification of potential molecular targets for breast cancer therapy.
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