Target intelligence / Profile preview

TP73 antisense RNA 1 (TP73-AS1)

Target
TP73-AS1
Molecular classification
Long non-coding RNA (lncRNA), Other (non-protein-coding transcript)
01

Overview

TP73 antisense RNA 1 (TP73-AS1, sometimes called KIAA0495 or PDAM) is a long non-coding RNA transcribed antisense to the TP73 gene at human chromosome 1p36.32. It acts primarily as a microRNA sponge, efficiently binding and sequestering human-specific miR-941 and other microRNAs such as miR-200, thereby modulating post-transcriptional gene regulation involved in cell migration, proliferation, and tumorigenesis. High expression of TP73-AS1 has been linked to adverse clinical outcomes and increased tumor grade in cancers such as glioma. TP73-AS1 holds promise as a biomarker for diagnosis and prognosis, and though not a conventional drug target (such as a receptor or enzyme), it represents a novel regulatory RNA molecule of increasing therapeutic interest in the context of oncology.

Other names
TP73-AS1KIAA0495PDAM (p53-dependent apoptosis modulator)
02

Mechanism of action

Not directly drugged; mechanism is via acting as a sponge for specific microRNAs, thereby regulating the downstream expression of their targets (e.g., tumor suppressors or oncogenes)

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Biological functions

MicroRNA sponge / competitive endogenous RNA (ceRNA) for miR-941 and miR-200Regulation of cell migration, proliferation, invasion, apoptosisRegulation of chemoresistance
04

Disease associations

Cancer (involved in multiple types: glioma, hepatocellular carcinoma, breast cancer, colorectal cancer, etc.)Other (potential generalized role in tumorigenesis)
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Safety considerations

Not directly applicable, as TP73-AS1 is not currently targeted by therapeutics; however, non-coding RNA targeting may present challenges such as off-target effects, delivery, and specificity
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Biomarkers

TP73-AS1 expression is a prognostic biomarker in several cancer types, especially glioma, correlating with tumor grade and patient survivalMay be used along with molecular subtypes (e.g., IDH mutation/1p/19q codeletion in glioma) for risk stratification

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