Long intergenic non-protein coding RNA p53-induced transcript (LINC-PINT)

Long intergenic non-protein coding RNA p53-induced transcript (LINC-PINT) is a long non-coding RNA induced by the p53 tumor suppressor protein, and is conserved between mouse and human[2][4][5]. In humans, LINC-PINT functions primarily as a tumor suppressor, being downregulated in multiple cancer types[1][2][5]. It is localized mainly in the nucleus and acts via direct interaction with the Polycomb repressive complex 2 (PRC2), especially its enzymatic subunit EZH2, to mediate H3K27 trimethylation and epigenetic silencing of target genes involved in cell proliferation and migration[1][2][4]. Additionally, LINC-PINT impedes DNA repair and enhances radiosensitivity by modulating ATM/ATR-Chk1/Chk2 signaling pathways[3]. It is also capable of encoding a short peptide (PINT87aa) that participates in suppression of glioblastoma proliferation by inhibiting transcription elongation of oncogenes[4]. Reduced expression of LINC-PINT is linked to increased malignancy and worse patient outcomes in several cancers, suggesting value as a prognostic biomarker[3][5]. There are currently no drugs directly targeting LINC-PINT; its mechanisms make it a potential, but as yet undrugged, therapeutic target[5].

Other names

Transcriptional regulator PINT87aaPINTTISPLFLJ43663PINT87aaLOC646329LincRNA-Pintp53-induced noncoding transcripttranscript induced by stressors from LINC-PINT locusMKLN1-AS1MKLN1 antisense RNA 1 (head to head)lincMkln1

Not targeted by drugs; functions via sponging miRNAs, recruiting chromatin modifiers (e.g., PRC2/EZH2), peptide translation (PINT87aa), and regulation of DNA repair pathways