microRNAs are important in cancer biogenesis and development. However, their underlying mechanisms in multiple myeloma (MM) are barely characterized. microRNA-20a (miR-20a) is a member of the microRNA-17-92 cluster. It has been implicated in various cancers, regulating the proliferation and invasion of cancer cells in vitro. Compared with healthy donors, it also has been reported to be elevated in plasma of MM patients. Here, we investigated the function of miR-20a. Our results showed that it promotes proliferation and inhibits apoptosis of MM cells in vitro by inhibiting early growth response protein 2. The effects of miR-20a were also evaluated in MM xenograft models of SCID/NOD mice. Apparent antitumor activity was achieved in xenograft mice injected with miR-20a inhibitor, while mimics of miR-20a significantly promoted tumor growth. These data indicate that miR-20a plays a crucial role in the biology of MM and represents a potential target for novel therapies for MM patients.
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http://dx.doi.org/10.2147/OTT.S143612 | DOI Listing |
N Engl J Med
January 2025
Centre Hospitalier Universitaire de Lille, Lille, France
N Engl J Med
January 2025
Tan Tock Seng Hospital, Singapore, Singapore
Target Oncol
January 2025
Berenson Cancer Center, West Hollywood, CA, USA.
Multiple myeloma (MM) is a bone-marrow-based cancer of plasma cells. Over the last 2 decades, marked treatment advances have led to improvements in the overall survival (OS) of patients with this disease. Key developments include the use of chemotherapy, immunomodulatory drugs, proteasome inhibitors, and monoclonal antibodies.
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January 2025
Department of Medicine, Mount Auburn Hospital, Harvard Medical School, 330 Mt Auburn St, Cambridge, MA 02138, USA.
J Immunother Cancer
January 2025
Rapa Therapeutics, Rockville, Maryland, USA.
Background: Polyclonal autologous T cells that are epigenetically reprogrammed through mTOR inhibition and IFN-α polarization (RAPA-201) represent a novel approach to the adoptive T cell therapy of cancer. Ex vivo inhibition of mTOR results causes a shift towards T central memory (T) whereas ex vivo IFN-α promotes type I cytokines, with each of these functions known to enhance the adoptive T cell therapy of cancer. Rapamycin-resistant T cells polarized for a type II cytokine phenotype were previously evaluated in the allogeneic transplantation context.
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