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Long intergenic non-protein coding RNA 2657 (LASTR) is a stress-induced lncRNA that regulates pre-mRNA splicing by modulating the interaction of SART3 with U4 and U6 small nuclear ribonucleoproteins (snRNPs) during spliceosome cycling[1]. LASTR is upregulated in several epithelial cancers, including breast cancer and lung adenocarcinoma, particularly under hypoxic conditions and in response to activation of the JNK/c-JUN pathway[1]. It acts as a principal regulator of gene expression and chromatin state, and has emerging importance as both a prognostic biomarker and a potential therapeutic target in oncology, particularly due to its influence on tumor immune escape and immunotherapy resistance[1][5][7]. No approved drugs or direct LASTR-targeting therapies currently exist, but its diagnostic and therapeutic relevance in oncology continues to be actively explored[1][5].
Not applicable (no approved drugs targeting LASTR directly as of current data)
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