NORAD (Non-Coding RNA Activated By DNA Damage)

ITPR3, MAPK1, and MAPK8 are biomarkers for meningioma, all targeted by SMAD3. Tamoxifen could treat meningioma by affecting paraptosis pathways, offering a promising basis for targeted therapy development.

High pretreatment NORAD expression is an independent risk factor for poor response to neoadjuvant chemotherapy. Downregulating NORAD restores oxaliplatin sensitivity in resistant cells.

NORAD is a promising diagnostic biomarker for ACS. Its correlation with inflammatory cytokines underlying its involvement in ACS pathogenesis.

NORAD was down-regulated in EC and affected the EC prognosis. NORAD overexpression facilitated YTHDF2-mediated m6A modification by interacting with FTO to elevate GPX4 degradation, thereby stimulating ECC ferroptosis and hindering EC progression.

However, NORAD with the sensitivity of 0.78 and negative predictive value of 70% performed better than the other transcripts in these two parameters. Taken together, MAPK14 and its related lncRNAs may have important roles in the pathogenesis of lung cancer.

In vivo tests confirmed that NORAD knockdown reduced MIRI in rats.Highly expressed NORAD promoted cardiomyocyte apoptosis and inflammatory responses. However, NORAD knockdown suppressed cardiomyocyte apoptosis to reduce MIRI through the miR-144-3p/TNRC6A axis.

Consequently, disruption of ALYREF LLPS leads to dissociation of the NARC1 complex, resulting in DNA damage and apoptosis in CMs. Collectively, these findings reveal a previously unrecognized mechanism by which DIC via interference with ALYREF condensates, offering new insight into the molecular basis of DIC.

DNA methyltransferase inhibitors (e.g., decitabine, guadecitabine) have shown promise in attenuating osteoclast differentiation, while histone deacetylase inhibitors display context-dependent effects on tumor progression and bone remodeling...Together, these advances position epigenetic modulation as a promising axis in precision oncology aimed at interrupting the pathological crosstalk between tumor cells and the bone microenvironment. This review synthesizes current mechanistic understanding, evaluates the therapeutic landscape, and outlines the translational challenges ahead in leveraging epigenetic science to prevent and treat bone metastases.

Lastly, application of anti-cancer treatment cisplatin, radiation, doxorubicin and PTX exhibited synergetic anti-cancer effect with NORAD knock-down, and NORAD over-expression attenuated anti-cancer effect of drugs. In total, NORAD is a promoter of oncogenesis and inhibited ferroptosis via miR-144-3p-mTOR-ferritinophagy in cancer cells.

NORAD upregulates SLC7A11 via the FUS/NR3C1 axis, thereby suppressing erastin-induced ferroptosis of BC cells.