Mirna Therapeutics, Inc., a leading developer of microRNA (miRNA)-based therapeutics, announced today the publication of new data in the journal Nature Medicine describing the role of the tumor suppressor miRNA, miR-34, in preventing cancer stem cell development. The published results reveal that miR-34 is commonly down-regulated in prostate cancer stem cells and that this down-regulation is essential for cancer stem cell viability. Systemic delivery of a miR-34 mimic inhibited tumor growth and metastasis in mice bearing prostate tumors. These new data support Mirna's previous publication in the journal Cancer Research that showed that the systemic delivery of a miR-34 mimic can inhibit tumor growth in mouse models of lung cancer.
“The collaborative effort with the Tang lab allowed us to establish a compelling link between miR-34 and cancer stem cell development”
The Nature Medicine publication resulted from a collaboration between scientists at Mirna Therapeutics and the University of Texas MD Anderson Cancer Center. The MD Anderson team was led by Dean Tang, M.D., Ph.D., Professor, Department of Carcinogenesis.
"The collaborative effort with the Tang lab allowed us to establish a compelling link between miR-34 and cancer stem cell development," said David Brown, Ph.D., Director of Research at Mirna Therapeutics. Our results suggest that the miR-34 mimic developed at Mirna might be particularly effective in combating the most aggressive cancer cells in patients."
"In the past year, Mirna Therapeutics has published four peer-reviewed articles demonstrating the therapeutic activity of tumor suppressor miRNAs in mouse models of cancer. Our published work has featured eight different cancer models and three different tumor suppressor miRNAs across multiple laboratories and provides compelling proof of concept for the robustness of miRNA replacement therapy," said Paul Lammers, M.D., President and CEO. "We are very pleased with our progress and look forward to moving our lead therapeutic candidates into clinical testing."
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