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RAS protein activator like 2 (RASAL2) is a member of the GAP1 family of GTPase-activating proteins that serves as a critical regulator of the Ras signaling pathway [1]. It functions by accelerating the intrinsic GTPase activity of Ras proteins, effectively switching them from an active, GTP-bound state to an inactive, GDP-bound state [1]. This activity dampens downstream proliferative signals, making it a key player in maintaining cellular homeostasis [2]. In the context of oncology, RASAL2 often functions as a tumor suppressor, and its loss or downregulation is associated with increased Ras activity and tumor progression in various malignancies, including breast and liver cancers [2]. Conversely, some studies suggest a context-dependent oncogenic role where RASAL2 promotes epithelial-mesenchymal transition and metastasis in specific subtypes like triple-negative breast cancer [3]. As a therapeutic target, RASAL2 mRNA is primarily explored through the lens of RNA interference (RNAi) and antisense oligonucleotide (ASO) technologies [4]. These approaches aim to either restore or inhibit expression depending on the specific cancer type and the functional role RASAL2 plays in that environment [4]. While no small molecules or biologics are currently FDA-approved for this target, it remains a significant biomarker for prognosis and treatment response in Ras-driven diseases [2].
RNA interference or antisense inhibition
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