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Colony stimulating factor 1 receptor (CSF-1R) mRNA is the transcript of the CSF1R gene, which encodes a type III receptor tyrosine kinase essential for the development and maintenance of the mononuclear phagocyte system. This mRNA is translated into the CSF-1R protein, which resides on the surface of macrophages, monocytes, and osteoclasts, responding to ligands like CSF-1 and IL-34 to drive cell survival and differentiation [1, 2]. In many solid tumors, the overexpression of CSF-1R mRNA leads to an abundance of tumor-associated macrophages (TAMs) that facilitate immune evasion and tumor progression [4]. Therapeutic targeting of the mRNA itself, rather than the resulting protein, is an emerging strategy using RNA interference (RNAi) or antisense oligonucleotides to silence gene expression at the source [3]. This approach aims to deplete immunosuppressive TAMs in the tumor microenvironment or modulate microglial activity in neurodegenerative conditions like ALSP [2, 4]. While protein-level inhibitors are more common, mRNA-targeted therapies offer high specificity and the potential for prolonged suppression of the CSF-1R signaling pathway.
mRNA degradation via RNA interference (RNAi) or antisense oligonucleotide (ASO) mediated cleavage, leading to reduced protein expression.
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