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Inhibition of Human Prostate Cancer Growth by Mesenchymal Stem Cells Delivering MiR‐16
Author(s) -
Jones Eyone,
Mazirka Pavel,
McNurlan Margaret A,
Brink Peter,
Caso Giuseppe
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb177
Subject(s) - mesenchymal stem cell , prostate cancer , in vivo , transfection , cancer , medicine , saline , cancer cell , cancer research , prostate , microrna , stem cell , pathology , cell culture , chemistry , biology , microbiology and biotechnology , biochemistry , genetics , gene
We have previously shown that miR‐16 has suppressive effects on the growth of human prostate cancer cells (PC3). However, one of the limitation for the use of inhibitory microRNAs (miRs) or small interfering RNAs (siRNA) for cancer therapy is effective delivery to cancer cells in vivo. The aim of this study was to evaluate the use of human mesenchymal stem cells (hMSC) as a potential in vivo delivery system for miRs to cancer cells. Human xenograft tumors were established by s.c. injection of 1 × 10 6 human prostate cancer cells (PC3) in immunocompromised nude mice. When tumors reached a measureable size, mice were randomized to receive hMSC previously transfected with miR‐16 (n=10, Treated) or saline (n=10, Control). 1 × 10 6 hMSC or saline were injected intratumorally. Tumor growth was assessed over a period of 3 weeks. Tumors in the group treated with hMSC transfected with miR‐16 showed a slower growth rate. After 3 weeks the average tumor volume was 40% lower in the treated group compared to controls (1.2 ± 0.22 vs. 2.04 ± 0.46 cm 3 ). The increment in tumor size over baseline (pre‐treatment) values was 5.0 fold in the treated and 8.4 fold in the control group (P<0.05). Tumor weight was also significantly lower in treated animals (0.82 ± 0.15 vs. 1.2 ± 0.16 g, P < 0.05). In summary, treatment of established xenograft tumors derived from human prostate cancer cells (PC3) with hMSC previously transfected with miR‐16 significantly slowed tumor growth. The results confirmed that miR‐16 can suppress tumor growth and indicate that hMSC could represent a suitable system for in vivo delivery. Support or Funding Information Supported by the Stony Brook Foundation TRO‐Catacosinos Cancer Translational Researcher Award, and by the Dept. of Surgery, Stony Brook University Medical Center (Small Grant Program)