ArticleBMC research notes2025
Impregnation of mesenchymal stem cell conditioned media with wortmannin enhanced its antiproliferative effect in breast cancer cells via PI3K/Akt/mTOR pathway.
Article in BMC research notes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Defining alteration in bone marrow mesenchymal stem cells (MSC) from acute myeloid leukemia and exploring cultured MSC-conditioned media as a novel anti-leukemia therapy agent.Cancer immunology, immunotherapy : CII · 2026Article
- Breast cancer stem cell activity driven byWorld journal of stem cells · 2026Article
- PI3 K/AKT/mTOR pathway and its role in breast cancer stem cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Long non-coding RNAs and autophagy: dual drivers of Hepatocellular carcinoma progression.Cell death discovery · 2025Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimConditioned media derived from Mesenchymal stem cells (MSC-CM) was suggested as a promising alternative cell-free regenerative therapy. It is hypothesized that the synergistic effect of MSC-CM with anticancer drugs may improve their antiproliferative and antimetastatic effects against cancer cells. Herein, the MSC-CM was impregnated with Wortmannin, a pan-PI3K/Akt/mTOR inhibitor, and their combined effect was investigated against breast cancer cells. MATERIALS AND
methodsTo explore this, the cytotoxic, apoptotic, and autophagic potentials were assessed in luminal-A breast cancer cells (MCF-7).
resultsWe found that incubation of MCF-7 to Wort-containing-CM induced apoptosis- and autophagy-mediated cell death, meanwhile prolonged exposure caused massive necrotic cell death. The involvement of MSC-CM effectively reduced Wortmannin IC50 observed in Wort-treated cells. Also, Wort-loaded-CM induced nuclear DNA fragmentation and reduced in vitro cell migration. These findings were associated with a Wort-dependent reduction in cell viability, the formation of the phosphorylated Akt and mTOR proteins, reduced the expression of mRNA, and downregulated the expression of the catalytic domain of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K-Ca).
conclusionThese findings revealed the promising antiproliferative and antimetastasis effects of combining pan-PI3K/Akt/mTOR inhibitors with MSC-derived-CM in breast cancer via the downregulation of PI3K/AKT/mTOR signaling pathways. Further studies are required to validate this chem-regenerative strategy in cancer treatment.
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