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Vascular endothelial growth factor C (VEGF-C) mRNA is the messenger RNA transcript that encodes the VEGF-C protein, a primary driver of lymphangiogenesis and a secondary mediator of angiogenesis [3, 9]. It functions by signaling through the VEGFR-3 and VEGFR-2 receptors to stimulate the growth and migration of endothelial cells [1, 14]. In many cancers, elevated levels of VEGF-C mRNA serve as a critical biomarker for lymph node metastasis and poor patient survival, as the resulting protein facilitates the expansion of lymphatic vessels that provide routes for tumor spread [2, 16]. Consequently, VEGF-C mRNA is a therapeutic target for RNA interference (RNAi) strategies, such as siRNAs and shRNAs, which aim to degrade the transcript and suppress pathological lymphangiogenesis [4, 12]. Conversely, synthetic VEGF-C mRNA is being investigated as a therapeutic agent for treating secondary lymphedema, where it is delivered to promote the regeneration of functional lymphatic networks [5, 7]. This dual role makes VEGF-C mRNA a focal point for both inhibitory oncology treatments and regenerative medicine [6, 8].
RNA interference (RNAi), Antisense-mediated mRNA degradation, and Exogenous mRNA translation (for mRNA-based therapy).
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