FOXD2-AS1 (FOXD2 Adjacent Opposite Strand RNA 1)

Our findings revealed that the YY1/FOXD2-AS1/EZH2 axis drives OSCC progression by epigenetically silencing CDKN1A. FOXD2-AS1 demonstrates potential as both a prognostic biomarker and therapeutic target, highlighting the need for further exploration of lncRNA-based therapeutic approaches in OSCC.

This study presents a novel migrasome-associated lncRNA risk signature with significant prognostic and therapeutic implications for ccRCC. The signature captures distinct immune, genomic, and pharmacologic features, and its core lncRNAs may promote tumor progression through migrasome-mediated signaling pathways, warranting further mechanistic investigation.

Despite their great potential, the clinical application exosomal ncRNAs remains limited. This review highlights recent advancements in exosomal ncRNA research and their potential as diagnostic markers, addressing both the opportunities and challenges for clinical implementation.

[This retracts the article DOI: 10.3727/096504019X15656904013079.].

Our results indicate that METTL3 regulates FOXD2-AS1 in an m6A-dependent manner through its interaction with YTHDF1, thereby influencing EC proliferation and apoptosis. This suggests a potential therapeutic target for the treatment of esophageal cancer.

On the whole, our innovative signature exhibits potential for prognostic prediction and assessment of immunotherapeutic response in patients with ccRCC.

In vitro and in vivo assays both confirmed that the FOXD2-AS1/MYC/EGLN3 axis could accelerate the progression of ccRCC. FOXD2-AS1 activated EGLN3 to accelerate ccRCC cell functions via binding to the transcription factor MYC.

These functions of lncRNA FOXD2-AS1 were attenuated by miR-324-3p inhibition. Our research demonstrated that FOXD2-AS1 silencing restrained cell growth and metastasis of OC via regulating miR-324-3p/SOX4 axis, indicating that lncRNA FOXD2-AS1 could be a novel potential therapeutic target for OC.

They have the potential to serve as novel biomarkers as they are detectable in bodily fluids and tissues. These findings enhance gallbladder treatments, mitigating resistance to chemo- and radiotherapy.

FOXD2-AS1 enhances OSCC malignant cell behaviors by interacting with miR-378 g to regulate CRABP2 expression.

In addition, it was found that the expression of PLOD1, p-Akt and p-mTOR proteins in OSCC cells was reduced by the inhibition of FOXD2-AS1, and FOXD2-AS1 and PLOD1 were closely related to the Akt/mTOR pathway. Increased expression of FOXD2-AS1 promotes OSCC growth, invasion and migration, which is important in part by targeting miR-185-5 p/PLOD1/Akt/mTOR pathway activity.

This research proposed that the dysregulation of lnc-FOXD2-AS1, CDC45, and CDK1 can contribute to both disease state and diagnosis as well as treatment. The present study proposes the future evolution of the functional role of lnc-FOXD2-AS1, CDC45, and CDK1 in AML development.