Target intelligence / Profile preview

Transcript inducer of AURKA lysosomal degradation (TIALD)

Target
TIALD
Molecular classification
Long non-coding RNA (lncRNA)
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Overview

Transcript inducer of AURKA lysosomal degradation (TIALD) is a long non-coding RNA that physically interacts with the oncoprotein Aurora kinase A (AURKA), promoting its degradation via the lysosomal pathway. TIALD expression is regulated by the m6A RNA methyltransferase METTL16: m6A-mediated methylation by METTL16 decreases TIALD stability and abundance in hepatocellular carcinoma. Loss of TIALD leads to increased AURKA levels, driving epithelial-mesenchymal transition (EMT), metastasis, and poor clinical outcomes. In HCC, TIALD has shown potential as both a prognostic biomarker and a therapeutic modulator: tumors with low TIALD expression may be more sensitive to the AURKA inhibitor alisertib. TIALD illustrates the emerging role of lncRNAs in regulating non-proteasomal protein degradation and cancer biology.

Other names
AC079360.1transcript that induced AURKA lysosomal degradationTIALD
02

Mechanism of action

Drugs targeting this pathway (like alisertib) block AURKA kinase activity; indirectly, TIALD enhances efficacy by promoting AURKA degradation

03

Biological functions

Regulation of protein degradation (specifically AURKA via the lysosomal pathway)Inhibition of metastasis (in hepatocellular carcinoma)Negative regulation of EMT (epithelial-mesenchymal transition)Putative involvement in cell proliferation and apoptosis (by modulating AURKA)
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Disease associations

Cancer (primarily hepatocellular carcinoma)Metastasis suppressionPrognosis marker (low expression is correlated with poor outcome in HCC)
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Safety considerations

Null (no specific safety concerns or therapeutic challenges related directly to TIALD reported in available sources; as a non-coding RNA, major therapeutic concern would be deliverability and specificity for gene therapy approaches)
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Interacting drugs

Alisertib
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Biomarkers

TIALD expression level (as a prognostic biomarker for HCC progression and therapeutic response to AURKA inhibitors)

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