HOTAIR (HOX Transcript Antisense RNA)

[This retracts the article DOI: 10.3727/096504017X15119467381615.].

Finally, while AQB significantly suppressed CSE-induced production of GM-CSF and CXCL8 in control AECs, it failed to do so in COPD. Together, these findings suggest that COPD-derived AECs are more susceptible to CSE-induced HOTAIR upregulation, which may have a pro-inflammatory effect that cannot be inhibited by AQB.

Our results suggest that H19 might be considered as a potential therapeutic target in LARC. Further studies with larger patient groups are required to confirm its diagnostic and prognostic utility.

Current pooled data suggest that selected HOTAIR variants - particularly rs920778 and rs4759314 - may contribute to inherited susceptibility to digestive system cancers, whereas rs1899663 and rs874945 appear unrelated in available datasets. Larger, well-designed studies across diverse ancestries and cancer sites are needed to confirm these findings and clarify potential gene-environment interactions.

Phytochemicals derived from Pithecellobium dulce, particularly oleanolic acid and rutin, emerge as promising selective modulators of AKT1 and AKT2, respectively. These findings provide a mechanistic and structural foundation for the development of isoform-guided AKT-targeted therapies and support further experimental validation toward precision oncology applications.

Furthermore, silencing of HOTAIR decreased PI3K/AKT phosphorylation, indicating pathway dependence. HOTAIR promotes the progression of B-ALL via the miR-326/IGF-1R axis and PI3K/AKT activation, suggesting its potential as a therapeutic target.

We further discuss translational applications of epigenetic biomarkers in liquid biopsies and targeted therapies (e.g., DNMT/HDAC inhibitors). Integrating multi-omics and epigenetic editing technologies may advance precision medicine in GC.

Future research should prioritize paired tumor-node lncRNA profiling, validation of FNAB-based molecular assays, and integration of multi-omics data for predictive modeling. Overall, integrating lncRNA analysis into ultrasound-guided fine-needle aspiration biopsy may enhance the detection of occult nodal metastases in head and neck squamous cell carcinoma and support more accurate nodal staging in clinically node-negative patients.

Moreover, it enables not only single-cell quantification and accurate discrimination of MALAT1 and HOTAIR in cancerous and normal breast tissues, but also rapid imaging of dual lncRNAs in living cells. This proof-of-concept work shows promising potential in clinical diagnostics and postoperative monitoring.

The quantitative evidence from numerous in vitro and in vivo studies has consistently demonstrated that flavonoid lncRNA modulation leads to a significant reduction in micro vessel density, expression of VEGF, and tumor burden. Improved bioavailability with more advanced nanoformulation and enhancement in preclinical validation of flavonoid lncRNA therapeutics, despite the remaining challenges like limited clinical data and off-target effects, offer low-toxicity targeted means of reprogramming tumor angiogenesis and overcoming resistance to the current therapies.

Although current research remains exploratory, lncRNAs show significant promise as predictive biomarkers and therapeutic targets. Future personalized strategies intergrating lncRNA profiles could help overcome drug resistance and improve patient outcomes.

These findings suggested that serum HOTAIR may be a potential diagnostic biomarker and that miR-646 may be a potential indicator of disease progression in EC. However, further validation in larger patient cohorts and investigation of exosomal expression levels are necessary in order to assess the potential clinical relevance and therapeutic potential of HOTAIR and miR-646.