FOXP1 overexpression

Notably, FOXP1 overexpression counteracted the suppressive effects induced by transfection with miRNA-22-3p mimic on HK-1 cell viability and migration. Therefore, these data indicate that miRNA-22-3p may be a clinically valuable biomarker for the therapy of NPC.

Mechanistically, FOXP1 could directly bind the IRF1 promoter, which triggered the transcriptional activity of IRF1. Taken together, FOXP1 suppressed PC growth via IRF1-dependent manner, serving as a potential prognostic biomarker for patients with PC.

XIST knockdown inhibited autophagy and carboplatin resistance of OC through FOXP1/protein kinase B (AKT)/mammalian target of rapamycin pathway by targeting miR-506-3p.

The cyclicity of circIFITM1 was confirmed by agarose gel electrophoresis and Sanger sequencing, and the stability of circIFITM1 was confirmed by actinomycin D assay...The overexpression of circIFITM1 downregulated miR-802 and upregulated FOXP1. circIFITM1 facilitates the proliferative and invasive abilities via miR-802/FOXP1 in Lovo cells.

Circ_OTUD7A promoted the progression of DLBCL by regulating the miR-431-5p/FOXP1 axis, which suggested that circ_OTUD7A might function as an oncogene in DLBCL.

Moreover, FOXP1 silencing via lentivirus or adeno-associated virus (AAV)-mediated delivery of shRNA suppressed osteosarcoma development and progression in cell-derived and patient-derived xenograft animal models. Taken together, we demonstrate that FOXP1, which is transactivated by ERK/JNK-c-JUN/c-FOS, drives osteosarcoma development by regulating the p53-P21/RB signaling cascade, suggesting that FOXP1 is a potential target for osteosarcoma therapy.

In summary, we identify FoxP1 as a novel repressor of skeletal muscle gene expression that is increased in cancer cachexia, whose up-regulation is sufficient to induce skeletal muscle wasting and weakness, and required for the normal wasting response to cancer.