Drug-releasing mesenchymal cells strongly suppress B16 lung metastasis in a syngeneic murine model
Open accessAbstract
BACKGROUND: Mesenchymal stromal cells (MSCs) are considered an important therapeutic tool in cancer therapy. They possess intrinsic therapeutic potential and can also be in vitro manipulated and engineered to produce therapeutic molecules that can be delivered to the site of diseases, through their capacity to home pathological tissues. We have recently demonstrated that MSCs, upon in vitro priming with anti-cancer drug, become drug-releasing mesenchymal cells (Dr-MCs) able to strongly inhibit cancer cells growth. METHODS: Murine mesenchymal stromal cells were loaded with Paclitaxel (Dr-MCsPTX) according to a standardized procedure and their ability to inhibit the growth of a murine B16 melanoma was verified by in vitro assays. The anti-metastatic activity of Dr-MCsPTX was then studied in mice injected i.v. with B16 melanoma cells that produced lung metastatic nodules. Lung nodules were counted under a dissecting stereomicroscope and metastasis investigated by histological analysis. RESULTS: We found that three i.v. injections of Dr-MCsPTX on day 5, 10 and 15 after tumor injection almost completely abolished B16 lung metastasis. Dr-MCsPTX arrested into lung by interacting with endothelium and migrate toward cancer nodule through a complex mechanism involving primarily mouse lung stromal cells (mL-StCs) and SDF-1/CXCR4/CXCR7 axis. CONCLUSIONS: Our results show for the first time that Dr-MCsPTX are very effective to inhibit lung metastasis formation. Actually, a cure for lung metastasis in humans is mostly unlikely and we do not know whether a therapy combining engineered MSCs and Dr-MCs may work synergistically. However, we think that our approach using Dr-MCs loaded with PTX may represent a new valid and additive therapeutic tool to fight lung metastases and, perhaps, primary lung cancers in human.
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Co-transplantation of paclitaxel-loaded BM-MSCs and acute lymphoblastic leukemia into immunodeficient nude mice resulted in complete inhibition of tumor formation.
“The co-transplantation of paclitaxel-loaded BM-MSCs and acute lymphoblastic leukemia into immunodeficient nude mice resulted in the complete inhibition of tumor formation, and the intra-tumoral injection of these drug-loaded MSCs led to a decrease in tumor size.”
From Mesenchymal Stem/Stromal Cells: Immunomodulatory and Bone Regeneration Potential after Tumor Excision in Osteosarcoma Patients (2023) · cites this paper as [114]
The Background (page unavailable) reports that prior co-injection and intratumoral injection of paclitaxel-loaded MSCs inhibited tumor growth. It does not specify acute lymphoblastic leukemia, immunodeficient nude mice, or complete prevention of tumor formation. This paper’s own experiment instead concerns B16 melanoma lung metastases in syngeneic mice. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe CM of paclitaxel-loaded BM-MSCs inhibited VEGF, a main player in tumor angiogenesis.
“Specifically, the CM of paclitaxel-loaded BM-MSCs inhibited VEGF, a main player in tumor angiogenesis [109,114].”
From Mesenchymal Stem/Stromal Cells: Immunomodulatory and Bone Regeneration Potential after Tumor Excision in Osteosarcoma Patients (2023) · cites this paper as [114]
The Methods section (no page number available) says conditioned medium from paclitaxel-loaded BM-derived mesenchymal cells was tested for inhibition of B16 melanoma-cell proliferation. The Discussion (no page number available) describes paclitaxel as anti-angiogenic, but the paper does not report that the conditioned medium inhibited VEGF (searched: VEGF and conditioned medium). (LLM, conf=0.74)
Experimental — accuracy not yet measuredThe CM of paclitaxel-loaded ASCs exhibited a dose-dependent effect on Ewing's sarcoma, prostate cancer, blastoma, neuroblastoma, and acute lymphoblastic leukemia cells.
“Also, the CM of paclitaxel-loaded ASCs exhibited a dose-dependent effect on Ewing’s sarcoma, prostate cancer, blastoma, neuroblastoma, and acute lymphoblastic leukemia cells.”
From Mesenchymal Stem/Stromal Cells: Immunomodulatory and Bone Regeneration Potential after Tumor Excision in Osteosarcoma Patients (2023) · cites this paper as [114]
The Results section reports that conditioned medium from paclitaxel-loaded SR4987 cells inhibited B16 melanoma proliferation in a dose-dependent manner. It does not report that effect for paclitaxel-loaded adipose-derived stromal cells (ASCs) or for the five cancer types listed in the claim. The paper’s Background identifies SR4987 as a bone-marrow-derived cell line; page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe CM of paclitaxel-loaded BM-MSCs completely inhibited the proliferation of prostate cancer, glioblastoma, acute lymphoblastic leukemia, malignant pleural mesothelioma, and multiple myeloma cells.
“whereas the CM of paclitaxel-loaded BM-MSCs completely inhibited the proliferation of prostate cancer, glioblastoma, acute lymphoblastic leukemia, malignant pleural mesothelioma, and multiple myeloma cells [109,114].”
From Mesenchymal Stem/Stromal Cells: Immunomodulatory and Bone Regeneration Potential after Tumor Excision in Osteosarcoma Patients (2023) · cites this paper as [114]
The Results section (page unavailable) says conditioned medium from paclitaxel-loaded, bone-marrow-derived SR4987 cells was tested for antiproliferative activity on MOLT-4 leukemia cells. It does not report complete inhibition of MOLT-4 proliferation, or this conditioned-medium result for prostate cancer, glioblastoma, malignant pleural mesothelioma, or multiple myeloma cells. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIntra-tumoral injection of drug-loaded MSCs led to a decrease in tumor size.
“The co-transplantation of paclitaxel-loaded BM-MSCs and acute lymphoblastic leukemia into immunodeficient nude mice resulted in the complete inhibition of tumor formation, and the intra-tumoral injection of these drug-loaded MSCs led to a decrease in tumor size.”
From Mesenchymal Stem/Stromal Cells: Immunomodulatory and Bone Regeneration Potential after Tumor Excision in Osteosarcoma Patients (2023) · cites this paper as [114]
Anti-cancer effects of drug-loaded MSCs are exerted via their conditioned medium (CM).
“Anti-cancer effects of drug-loaded MSCs are exerted via their conditioned medium (CM).”
From Mesenchymal Stem/Stromal Cells: Immunomodulatory and Bone Regeneration Potential after Tumor Excision in Osteosarcoma Patients (2023) · cites this paper as [114]
Ewing's sarcoma was the most sensitive to the CM of paclitaxel-loaded ASCs compared to the other cancer cells.
“Ewing’s sarcoma was the most sensitive to the CM of paclitaxel-loaded ASCs compared to the other cancer cells [109,114].”
From Mesenchymal Stem/Stromal Cells: Immunomodulatory and Bone Regeneration Potential after Tumor Excision in Osteosarcoma Patients (2023) · cites this paper as [114]
The Methods section tests conditioned medium from paclitaxel-loaded murine marrow stromal cells against B16 melanoma, not medium from adipose-derived stromal cells (ASCs) against multiple cancers. A Background passage mentions anti-tumor activity in paclitaxel-loaded adipose-derived cells, but our copy does not report a comparison showing Ewing’s sarcoma was the most sensitive. Searches for Ewing’s sarcoma, ASC conditioned medium, and comparative sensitivity found no supporting passage. (LLM, conf=0.73)
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- Authors
- Pessina, A., Leonetti, C., Artuso, S., Benetti, A., Dessy, E., Pascucci, L., Passeri, D., Orlandi, A., Berenzi, A., Bonomi, A., Coccè, V., Ceserani, V., Ferri, A., Dossena, M., Mazzuca, P., Ciusani, E., Ceccarelli, P., Caruso, A., Portolani, N., Sisto, F., Parati, E., & Alessandri, G.
- Affiliations
- University of Milan (IT)
- Instituto Nazionale Tumori Regina Elena (IT)
- University of Brescia (IT)
- University of Perugia (IT)
- University of Rome Tor Vergata (IT)
- Fondazione IRCCS Istituto Neurologico Carlo Besta (IT)
- Corresponding author
- Pessina, Augusto
- ORCID
- Venue
- Journal of Experimental & Clinical Cancer Research
- Published
- 2015-08-13
- Volume
- 34
- Issue
- 1
- Pages
- 82-82
- ISSN
- 0392-9078 (ISSN-L)
- 1756-9966
- PMC
- PMC4534150
- OpenAlex
- W2165264327
- Cited by
- 39
- References
- 55
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 5 · 2023: 3 · 2022: 3 · 2021: 3 · 2020: 6 · 2019: 4 · 2018: 7 · 2017: 3 · 2016: 3
- FWCI
- 2.43
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Journal of Experimental & Clinical Cancer Research (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
- Institutional Research Information System (Università degli Studi di Brescia) (submittedVersion, other-oa)
- Funders
- Associazione Italiana per la Ricerca sul Cancro (IT) (14337)
- Topics
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biotechnology › Cancer Research and Treatments
- Keywords
- mesenchymal stem cells, paclitaxel, B16 melanoma, lung metastasis, anti-metastatic therapy, lung stromal cells, cell migration, syngeneic murine model, cell-mediated drug delivery
- MeSH terms
- Animals, Disease Models, Animal, Humans, Lung Neoplasms, Male, Melanoma, Experimental, Mice, Inbred C57BL, Neoplasm Metastasis, Drug Delivery Systems, Mice, Mesenchymal Stem Cells
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