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TPM1 antisense RNA (TPM1-AS or TPM1-AS1) is a long non-coding RNA (lncRNA) transcribed antisense to the TPM1 (tropomyosin 1) gene[9][3][7]. TPM1-AS regulates the alternative splicing of the tropomyosin 1 gene via physical interaction with RNA-binding proteins, most notably RBM4, resulting in exon skipping that decreases production of pro-migratory TPM1 isoforms in cancer cells[1][3][5]. In human esophageal cancer, increased TPM1-AS expression leads to inhibited cell migration and reduced filopodia formation, suggesting a tumor-suppressive function[1][3]. TPM1-AS also regulates the expression of other genes via competition with microRNAs (such as hsa-miR-503-5p and hsa-miR-92a-1-5p for BCAR1 binding)[3]. SNPs in the TPM1-AS locus and its expression patterns have been proposed as possible biomarkers for some cancers[3]. There are currently no known drugs directly targeting TPM1-AS, and it is not classified as a classical therapeutic target such as a receptor, enzyme, or transporter.
Not applicable; no therapeutically targeted drugs identified. Its functional activity is by interaction with RNA-binding proteins (such as RBM4 and, possibly, YBX1), altering the splicing of tropomyosin 1 (TPM1) and possibly other targets[1][3][5]. Competes with certain miRNAs for binding, which in turn can regulate genes such as BCAR1[3].
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