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Fibroblast activation protein alpha (FAP) mRNA is the messenger RNA transcript encoding the FAP protein, a type II transmembrane serine protease that is highly upregulated in activated fibroblasts, particularly cancer-associated fibroblasts (CAFs) [1][2]. While FAP expression is nearly undetectable in most healthy adult tissues, its mRNA is abundantly present in the stroma of over 90% of epithelial cancers and in various fibrotic conditions, making it a highly selective therapeutic target [4][5]. Targeting FAP mRNA through RNA interference (RNAi) or antisense oligonucleotides (ASOs) aims to reduce the production of the FAP protein, thereby disrupting the pro-tumorigenic and immunosuppressive environment created by CAFs [4]. Additionally, FAP mRNA is being utilized in the development of mRNA vaccines to induce T-cell mediated immunity against the tumor stroma and in innovative in vivo CAR-T cell therapies [3]. By modulating the expression of FAP at the transcript level, these strategies seek to enhance the delivery of chemotherapeutic agents and improve the overall efficacy of cancer immunotherapies [5].
RNA interference (RNAi) leading to the sequence-specific degradation of the FAP transcript to downregulate protein expression, or utilization as a template for the expression of FAP antigens to stimulate an anti-stromal immune response.
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