FOXP2 (Forkhead Box P2)

The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 20: 3149‑3159, 2019; DOI: 10.3892/mmr.2019.10563].

Overexpression of RBM15B or KDM4C attenuated ferroptosis and reversed the suppression of HCC cell growth induced by FOXP2 overexpression. In conclusion, FOXP2 may promote ferroptosis and inhibit cell proliferation in HCC by decreasing SLC7A11 expression via the RBM15B/KDM4C axis in an m6A-dependent manner.

A panel of four serum miRNAs (hsa-miR-107, hsa-miR-146a-5p, hsa-miR-15b-5p, and hsa-miR-218-5p) exhibits high specificity and sensitivity. It shows potential as an efficient, non-invasive, and cost-effective biomarker for BC screening.

The compensatory expression of Twist1 in FOXP2-overexpressing breast cancer cells counteracted FOXP2's inhibitory effects on the stemness of breast cancer cells. Together, the results showed that FOXP2 attenuated the stemness of breast cancer cells by abolishing the transcription of Twist1.

The peptide group molecules, Phospholipase A2, Klotho protein, and soluble urokinase plasminogen activator receptor (suPAR), also remain consistently important. From the perspective of SZ as a disease associated with neuronal damage, biomarkers correlating with brain injury, neuron-specific enolase (NSE), and S100B protein should be considered.

Notably, AKT activation enhanced FOXP2 expression, indicating a FOXP2/SOS1/AKT negative feedback loop. Collectively, our findings suggest that FOXP2 inhibits proliferation in KRAS-mutant CRC by suppressing SOS1-mediated PI3K/AKT signaling, and may serve as a prognostic biomarker and potential therapeutic target in KRAS-driven CRC.

Collectively, this study establishes FBXW2 as a critical tumor suppressor in GC, operating through ubiquitin-mediated degradation of WASL to inhibit cancer progression. Targeting the FOXP2-FBXW2-WASL axis may represent a promising therapeutic strategy for combating GC malignancy.

Integrated genomic, transcriptomic, and immune repertoire analyses reveal that bats employ distinct antiviral strategies, primarily mediated by enhanced immune tolerance and suppressed inflammatory responses. This review provides foundational information, collaboration directions, and new perspectives for various laboratories conducting basic and applied research on the vast array of bat biology.

Rescue experiments further confirmed that FOXP2 transcriptionally activated ZSCAN18 and thus inhibited stemness and tumor growth. Collectively, FOXP2 mediates ZSCAN18 transcriptional activation to inhibit OSCC by blocking Hedgehog signaling.

The addition of the MYLK-specific inhibitor ML-7 reversed the effect of FOXP2 overexpression on the invasion and migration of EC cells. FOXP2 suppresses the proliferation, invasion, and migration of EC cells through the activation of MYLK.

Down regulation of these genes occurred in SV2C- and somatostatin-expressing interneurons, oligodendrocytes, and oligodendrocyte precursor cells. These results support the value of gene regulation studies for the evolution of human cognitive abilities and the neuropsychiatric disorders that accompany it.

Furthermore, NFYB and FOXP2 are identified as activators of PROS1 transcription in fibroblasts, promoting PTMC progression through the MERTK/WNT/TGF-β signaling. These findings underscore the PROS1/MERTK axis as a critical component of the cellular microenvironment and a key regulatory mechanism in PTMC progression.