Genetically modified mesenchymal stromal cells in cancer therapy

Sage, EK; Thakrar, Ricky; Janes, Sam M.

doi:10.1016/j.jcyt.2016.09.003

Cited by 102 publications

(68 citation statements)

References 114 publications

(123 reference statements)

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“…MSCs are multipotent stem cells with self‐renewal property that, under a specific condition, can differentiate into various specialized cell types. A growing body of research has paid attention toward using MSCs in cell and gene therapies, which underscores the potential usage of MSCs in the clinic . However, transfer of exogenous genes into the MSCs remains a challenge.…”

Section: Discussionmentioning

confidence: 99%

A simple and highly efficient method for transduction of human adipose‐derived mesenchymal stem cells

Bolandi

Rad

Soudi

et al. 2018

J of Cellular Biochemistry

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Mesenchymal stem cells (MSCs) are multipotent cells capable of differentiating into a wide range of cell types and provide a potential to transfer therapeutic protein in vivo, making them valuable candidates for gene therapy and cell therapy. However, using MSCs in in vivo is limited due to the low rate of transfection and transduction efficacy. Therefore, developing methods to efficiently transfer genes into MSCs would provide a number of opportunities for using them in the clinic. Here, we introduce a simple and robust method for efficient transduction of human adipose‐derived MSCs by modification under the culture condition of human embryonic kidney cells 293 (HEK293T) and MSCs. Moreover, as a transduction enhancer, polybrene was replaced with Lipofectamine, a cationic lipid. Therefore, we showed that transduction of primary cells can be increased efficiently by modifying the culture condition.

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Section: Discussionmentioning

confidence: 99%

A simple and highly efficient method for transduction of human adipose‐derived mesenchymal stem cells

Bolandi

Rad

Soudi

et al. 2018

J of Cellular Biochemistry

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“…Similarly, engineering MSCs to express TNF‐related apoptosis‐inducing ligand (TRAIL) has shown particular promise in multiple preclinical cancer models . This preclinical data together with decades of clinical observations regarding MSC biodistribution patterns led to the recently initiated TACTICAL trial, a phase I/II study of MSC‐TRAIL in combination with cisplatin and pemetrexed in non‐small cell lung cancer (NSCLC) patients [NCT03298763] . Previous efforts using systemic delivery of TRAIL as an anti‐cancer strategy failed clinical testing due to toxicity and poor responses at the administered doses .…”

Section: Msc‐based Anti‐cancer Strategiesmentioning

confidence: 99%

Concise Review: Mesenchymal Stem Cell-Based Drug Delivery: The Good, the Bad, the Ugly, and the Promise

Krueger

Thorek

Denmeade

et al. 2018

Stem Cells Translational Medicine

205

163

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The development of mesenchymal stem cells (MSCs) as cell‐based drug delivery vectors for numerous clinical indications, including cancer, has significant promise. However, a considerable challenge for effective translation of these approaches is the limited tumor tropism and broad biodistribution observed using conventional MSCs, which raises concerns for toxicity to nontarget peripheral tissues (i.e., the bad). Consequently, there are a variety of synthetic engineering platforms in active development to improve tumor‐selective targeting via increased homing efficiency and/or specificity of drug activation, some of which are already being evaluated clinically (i.e., the good). Unfortunately, the lack of robust quantification and widespread adoption of standardized methodologies with high sensitivity and resolution has made accurate comparisons across studies difficult, which has significantly impeded progress (i.e., the ugly). Herein, we provide a concise review of active and passive MSC homing mechanisms and biodistribution postinfusion; in addition to in vivo cell tracking methodologies and strategies to enhance tumor targeting with a focus on MSC‐based drug delivery strategies for cancer therapy. Stem Cells Translational Medicine 2018;1–13

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“…MSCs potentially support tumor development through immune suppression, epithelial mesenchymal transition, angiogenesis, and serve as cancer stromal cells [1][2][3]. It is verified that bone marrow MSCs is the main source of carcinoma associated fibroblasts in breast cancer microenvironment [3].…”

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: Lack of miR-216b-5p, miR-33a-5p or miR-122-5p in MSCs exosomes promotes breast cancer glycolysis by targeting HK2, LDHA and PKM2

Xia¹,

Yu²,

Mao³

et al. 2018

Oncotarget

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Exosomes contain many important components including miRNAs for cancerstromal communication. Mesenchymal stromal cells support tumor development, however, the low expression of miRNAs in exosomes and their regulation roles from mesenchymal stromal cells are still unclear. In this study, we hypothesized that mesenchymal stromal cells-derived exosomes promote breast cancer cell glycolysis. Our results showed that mesenchymal stromal cells-derived exosomes promoted cell proliferation and glycolysis of breast cancer cells. Furthermore, sequencing of exosomal RNAs revealed miR-216b-5p, miR-33a-5p and miR-122-5p were lack of expression in exosomes from mesenchymal stromal cells. MiR-216b-5p, miR-33a-5p and miR-122-5p overexpression in breast cancer cells suppressed glycolysis by targeting HK2, LDHA and PKM2 respectively. These results provided valuable insights and mechanism of mesenchymal stromal cells-secreted exosomes on the glycolysis of breast cancer.

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Genetically modified mesenchymal stromal cells in cancer therapy

Cited by 102 publications

References 114 publications

A simple and highly efficient method for transduction of human adipose‐derived mesenchymal stem cells

A simple and highly efficient method for transduction of human adipose‐derived mesenchymal stem cells

Concise Review: Mesenchymal Stem Cell-Based Drug Delivery: The Good, the Bad, the Ugly, and the Promise

WITHDRAWN: Lack of miR-216b-5p, miR-33a-5p or miR-122-5p in MSCs exosomes promotes breast cancer glycolysis by targeting HK2, LDHA and PKM2

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