miR-203–SOCS3 pathway

The **miR-203–SOCS3 pathway** refers to the regulatory interaction between microRNA-203 and its direct target, suppressor of cytokine signaling 3 (SOCS3). miR-203 is a microRNA strongly expressed in epithelial tissues such as the skin, and can also circulate systemically[2][6]. It binds to the 3′-UTR of SOCS3 mRNA, leading to its degradation or translational repression, and thus reduces SOCS3 protein levels[1][4][6]. SOCS3 is a negative regulator of the JAK/STAT and NF-κB signaling pathways; decreasing SOCS3 with miR-203 increases pathway activity, promoting inflammatory cytokine production and cell proliferation. This axis plays a notable role in: - **Psoriasis:** miR-203 suppresses SOCS3, contributing to VEGF overexpression and pathological angiogenesis[1][2]. - **Breast cancer:** miR-203-mediated repression of SOCS3 supports cancer cell growth and chemoresistance; anti-miR-203 therapy restores SOCS3, suppressing stemness and proliferation[3][5]. - **Epilepsy/neuroinflammation:** Exosomal miR-203 from bone marrow stem cells downregulates SOCS3 and activates NF-κB, influencing the neuroinflammatory environment[4]. The pathway is not a single protein or receptor, but a regulatory axis involving a non-coding RNA and a signaling protein; the term “miR-203–SOCS3 pathway” is non-canonical as a molecular drug target (not a unique molecule), thus the target name is structurally incorrect for standard pharmacological catalogs. Nevertheless, both miR-203 and SOCS3 are individually considered investigational therapeutic targets for disorders involving inflammation, cancer, and autoimmune responses[3][5][6].

Other names

miR-203/SOCS3 axismiR-203–SOCS3 signalingmicroRNA-203–suppressor of cytokine signaling 3 pathway

miR-203 inhibition (anti-miR-203) increases SOCS3 expression, downregulates JAK/STAT/NF-κB signaling, reduces cytokine production and cell proliferation. miR-203 mimics suppress SOCS3, upregulate JAK/STAT/NF-κB signaling, promote inflammation and proliferation.