FGFRL1 (Fibroblast Growth Factor Receptor Like 1)

Our findings provide novel insights into OC molecular mechanisms and highlight promising therapeutic targets, establishing a foundation for future research and clinical applications.

Functional assays demonstrated FGFRL1's oncogenic role, showing G1 phase arrest, and reduced proliferation, migration, and invasion (P < 0.001). Our study highlights FGFRL1 as a key driver of EC progression.

The present review summarizes the research progress of FGFRL1, especially its subcellular location, molecular function, and associated human disease. These data may offer valuable resources for further studying the molecular function of FGFRL1 and disclosing the mechanism of its related human diseases.

And THP-M2 increased the tumor volume and MDR, YB-1, BCRP, p-PI3K, p-AKT, and p-mTOR levels. Overall, miR-210 from PC stem cell-derived exosome targets and inhibits FGFRL1 to promote macrophage M2 polarization, which activates the p-PI3K/p-AKT/p-mTOR pathway and increases GEM resistance.

Moreover, combined with the results of the rescue experiment, VPS9D1-AS1 was found to upregulate FGFRL1 by competitively sponging miR-187-3p to accelerate the malignant behaviors of prostate cancer cells. In conclusion, VPS9D1-AS1 could promote the phenotype progression of prostate cancer cells through targeting the miR-187-3p/FGFRL1 axis, and it has the potential to be a target for prostate cancer patients.

In this study, we found that MMP-2 plays a significant role in AML progression and may serve as a potential prognostic biomarker and therapeutic target for the effective management of AML.