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Terminal nucleotidyltransferase 5C (TENT5C) is a non-canonical poly(A) RNA polymerase that preferentially catalyzes the addition of adenosine to A-rich mRNA substrates, stabilizing them and modulating their expression, especially those encoding endoplasmic reticulum-targeted proteins and immunoglobulin in plasma cells[1][2][4][10]. TENT5C acts as a tumor suppressor by restraining the activity of Polo-like kinase 4 (Plk4), thereby limiting excessive centriole duplication and suppressing cell proliferation and cancer invasion, particularly in multiple myeloma and other plasma cell-related malignancies[1][2][8]. It is genomically located at chromosome 1p12; deletions or mutations are associated with decreased survival in myeloma patients[2][5][8]. TENT5C also shows molecular interactions involving the secretory pathway, endoplasmic reticulum-associated proteins, and nuclear hormone receptor activity[2][3]. While it has strong relevance as a potential therapeutic target and biomarker in cancer, there are currently no drugs approved or documented to interact directly with TENT5C[2][8].
Not applicable due to lack of direct drug interactions; mechanisms generally relate to modulation of mRNA polyadenylation and suppression of oncogenic kinase activity
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