FOXD3-AS1 (FOXD3 Antisense RNA 1)

FOXD3-AS1 influences PCa cell behavior via the miR-491-5p/PEG10 axis.

We identified a novel risk signature consisting of four PRlncRNAs, which is an independent prognostic indicator for patients with COAD. This PRlncRNA risk signature is potentially relevant for immunotherapy and could serve as a therapeutic target for COAD.

In vivo experiments showed that CD8+T cell-derived exosome miR-2682 inhibited lung cancer tumor formation, while CAF-derived exosome FOXD3-AS1 promoted lung cancer tumor formation. This study provides mechanistic insights into the role of miR-2682 and FOXD3-AS1 in lung cancer progression and provides new strategies for lung cancer treatment.

Altogether, our study suggests a possible role of lincRNA-p21 and RMST lncRNAs in the etiology of PC pathobiology, and their biomarker role may be understood in future studies.

FOXD3-AS1 facilitates the CCND1-driven progression of glioblastoma by serving as a competing endogenous RNA (ceRNA) for miR-3918. This suggests that FOXD3-AS1 may be a potential therapeutic target for the management of glioblastoma development.

Interfering with lncRNA F-A level can upregulate M expression. Silencing of lncRNA F-A can inhibit PMI of NPC cells.

FOXD3-AS1 was a sponge of miR-128-3p through upregulating IGF2BP3 in glioma. Our findings shed light on diagnosis and treatment of glioma.

The expression levels of these lncRNAs were significantly higher in glioblastoma cell lines than in normal cells. Our study shows that the signature of 17 lncRNAs related to genomic instability has prognostic value for gliomas and could provide a potential therapeutic method for glioblastoma.

Each group of meningiomas displayed a unique gene expression signature suggesting signaling pathways potentially implicated in tumorigenesis. These findings will improve our understanding of meningioma tumorigenesis and prognosis.

FOXD3-AS1 is significantly upregulated in LC tissues and plasma. FOXD3-AS1 could be a potential biomarker for LC subtype identification and early diagnosis.

In summary, our results reported the regulatory mechanism of FOXD3-AS1 in breast cancer progression by targeting miR-127-3p/ARF6 axis to affect cell proliferation, migration, invasion and tumor growth.

Importantly, depletion of WEE1 could reverse TMZ resistant phenotype in FOXD3-AS1-overexpressed GBM cells. Collectively, our findings reveal a critical role of FOXD3-AS1 in the survival of GBM cells and TMZ resistance, which suggests that FOXD3-AS1 is a potential biomarker for the diagnosis and treatment of GBM.