Immunoproapoptotic molecule scFv-Fdt-tBid modified mesenchymal stem cells for prostate cancer dual-targeted therapy

Fu, Yan; Li, Xia; Li, Nan; Zhang, Rui; Wang, Qinhao; Yi, Ruokun; Hao, Xiaoke; Ni, Jianxin; Wang, He; Wu, Guojun

doi:10.1016/j.canlet.2017.05.003

Cited by 13 publications

(11 citation statements)

References 55 publications

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“…Moreover, MSCs, possessing an inherent tropism for sites of inflammation, recurrently exist in sites of cancer, including prostatic lesions 7 . Additionally, MSCs are demonstrated to act as cytokines or a delivery vehicle of anti-tumor drugs to participate in the treatment of prostate cancer 8 …”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Exosomes Derived from miR-143-Overexpressing MSCs Inhibit Cell Migration and Invasion in Human Prostate Cancer by Downregulating TFF3

Che

Shi

et al. 2019

Molecular Therapy - Nucleic Acids

126

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Exosomes are membrane-enclosed nanovesicles that shuttle active cargoes, such as mRNAs and microRNAs (miRNAs), between different cells. Mesenchymal stem cells (MSCs) are able to migrate to the tumor sites and exert complex functions over tumor progress. We investigated the effect of human bone marrow-derived MSC (BMSC)-derived exosomal miR-143 on prostate cancer. During the co-culture experiments, we disrupted exosome secretion by the inhibitor GW4869 and overexpressed exosomal miR-143 using miR-143 plasmid. miR-143 was involved in the progression of prostate cancer via trefoil factor 3 (TFF3). Moreover, miR-143 was downregulated while TFF3 was upregulated in prostate cancer cells and tissues, and miR-143 was found to specifically inhibit TFF3 expression. Human MSC-derived exosomes enriched miR-143 and transferred miR-143 to prostate cancer cells. Furthermore, elevated miR-143 or exosome-miR-143 or silencing TFF3 inhibited the expression of TFF3, proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP)-2, and MMP-9 and PC3 cell proliferation, migration, invasion, and tumor growth, whereas it promoted apoptosis. In conclusion, hMSC-derived exosomal miR-143 directly and negatively targets TFF3 to suppress prostate cancer.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Exosomes Derived from miR-143-Overexpressing MSCs Inhibit Cell Migration and Invasion in Human Prostate Cancer by Downregulating TFF3

Che

Shi

et al. 2019

Molecular Therapy - Nucleic Acids

126

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“…CM-FDMSC contains factors that reduce various aspects of tumorigenicity of A375 melanoma cells. We confirmed that CM-FDMSC inhibits A375 melanoma cell expansion by inducing apoptosis of A375 melanoma cells, rather than inhibiting the proliferation, consistent with previous reports 29. In addition, migration and invasion abilities of A375 melanoma cells were suppressed by CM-FDMSC in both the monolayer wound healing and transwell invasion assays and again were consistent with previous reports 30.…”

Section: Discussionsupporting

confidence: 92%

<p>Antitumor effects of conditioned media of human fetal dermal mesenchymal stem cells on melanoma cells</p>

BenCheng¹,

Wang²,

Pan³

et al. 2019

OTT

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Background: Malignant melanoma is the most lethal form of cutaneous tumor and has a high metastatic rate and motility capacity. Owing to the poor prognosis, it is urgent to seek an effective therapeutic regimen. Human mesenchymal stem cells (MSCs) can home to tumor cells and have been shown to play important roles in both promoting and inhibiting tumor development. Fetal dermal MSCs (FDMSCs), derived from fetal skin are a novel source of MSCs. Nevertheless, the antitumor capacity of FDMSCs on malignant melanoma is not clearly understood. Materials and methods: FDMSCs were extracted from the dorsal skin of fetal tissues. A375 melanoma cells lines were obtained from American Type Culture Collection. The effects of conditioned media from FDMSCs (CM-FDMSC) on A375 melanoma cells were tested in vivo using tumor formation assay and in vitro using cell viability, 5-ethynyl-2ʹ-deoxyuridine incorporation, flow cytometry, TdT-mediated dUTP Nick-End Labeling (TUNEL), wound healing, transwell invasion, and Western blotting. Results: CM-FDMSC inhibited A375 tumor formation in vivo. In vitro, CM-FDMSC inhibited the tumor-related activities of A375 melanoma cells, as evidenced reductions in viability, migration, and invasion. CM-FDMSC-treated A375 cells showed decreased phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), and extracellular signal-regulated kinase (ERK) phosphorylation, and up-regulation of Bcl-2-Associated X (BAX) and down-regulation of B-cell lymphoma-2 (BCL-2) expression. Conclusion: CM-FDMSC can inhibit the tumor-forming behaviors of A375 melanoma cells and inhibit PI3K/AKT and mitogen-activated protein kinase signaling to shift their BCL-2/BAX ratio toward a proapoptotic state. Identification of the bioactive components in CM-FDMSC will be important for translating these findings into novel therapies for malignant melanoma.

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“…The genetic modification of the MSCs was achieved using different approaches, including viral and non-viral approaches. The types of viral vectors used for MSC genetic manipulation include the following: adenovirus (Chang et al, 2003(Chang et al, , 2004Tsuchida et al, 2003;Chen et al, 2008;Fritz et al, 2008;Jiang et al, 2009;Xin et al, 2009;Gao et al, 2010;Huang et al, 2010;Zhang et al, 2010;Zhao et al, 2010;Kosaka et al, 2012;Wang et al, 2012;Kim et al, 2013), lentivirus (Sasportas et al, 2009;Luetzkendorf et al, 2010;Bak et al, 2011;Seo et al, 2011;Zhang et al, 2011;Fei et al, 2012;Zolochevska et al, 2012;Ahn et al, 2013;Lee et al, 2013;Martinez-Quintanilla et al, 2013;Yan et al, 2013Yan et al, , 2017Fransson et al, 2014;Niu et al, 2014;Qi et al, 2015;Wang et al, 2015b;Amara et al, 2016;Beegle et al, 2016), retrovirus (Kucerova et al, 2007(Kucerova et al, , 2008(Kucerova et al, , 2014Cavarretta et al, 2010;Altanerova et al, 2012;Zou et al, 2012;Martinez-Quintanilla et al, 2013;Abrate et al, 2014;…”

Section: Resultsmentioning

confidence: 99%

Enhancement of the Therapeutic Capacity of Mesenchymal Stem Cells by Genetic Modification: A Systematic Review

Pawitan

Bui

Mubarok

et al. 2020

Front. Cell Dev. Biol.

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Background: The therapeutic capacity of mesenchymal stem cells (also known as mesenchymal stromal cells/MSCs) depends on their ability to respond to the need of the damaged tissue by secreting beneficial paracrine factors. MSCs can be genetically engineered to express certain beneficial factors. The aim of this systematic review is to compile and analyze published scientific literatures that report the use of engineered MSCs for the treatment of various diseases/conditions, to discuss the mechanisms of action, and to assess the efficacy of engineered MSC treatment. Methods:We retrieved all published studies in PubMed/MEDLINE and Cochrane Library on July 27, 2019, without time restriction using the following keywords: "engineered MSC" and "therapy" or "manipulated MSC" and "therapy." In addition, relevant articles that were found during full text search were added. We identified 85 articles that were reviewed in this paper.Results: Of the 85 articles reviewed, 51 studies reported the use of engineered MSCs to treat tumor/cancer/malignancy/metastasis, whereas the other 34 studies tested engineered MSCs in treating non-tumor conditions. Most of the studies reported the use of MSCs in animal models, with only one study reporting a trial in human subjects. Thirty nine studies showed that the expression of beneficial paracrine factors would significantly enhance the therapeutic effects of the MSCs, whereas thirty three studies showed moderate effects, and one study in humans reported no effect. The mechanisms of action for MSC-based cancer treatment include the expression of "suicide genes," induction of tumor cell apoptosis, and delivery of cytokines to induce an immune response against cancer cells. In the context of the treatment of non-cancerous

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Immunoproapoptotic molecule scFv-Fdt-tBid modified mesenchymal stem cells for prostate cancer dual-targeted therapy

Cited by 13 publications

References 55 publications

RETRACTED: Exosomes Derived from miR-143-Overexpressing MSCs Inhibit Cell Migration and Invasion in Human Prostate Cancer by Downregulating TFF3

RETRACTED: Exosomes Derived from miR-143-Overexpressing MSCs Inhibit Cell Migration and Invasion in Human Prostate Cancer by Downregulating TFF3

<p>Antitumor effects of conditioned media of human fetal dermal mesenchymal stem cells on melanoma cells</p>

Enhancement of the Therapeutic Capacity of Mesenchymal Stem Cells by Genetic Modification: A Systematic Review

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