Xenograft experiments confirmed that circRAPGEF5 knockdown suppressed FGFR1-mediated tumor growth by promoting miR-198 expression. circRAPGEF5 acts as a tumor promoter via a novel circRAPGEF5/miR-198/FGFR1 axis, providing a potential biomarker and therapeutic target for the management of PTC.
Amplified Crosstalk Between Estrogen Binding and GFR Signaling Mediated Pathways of ER Activation Drives Responses in Tumors Treated with Endocrine Disruptors.
Then we subgroup the patients with GFR ≥ 90 mg/min/1.73 m<sup>2</sup>, to exclude the effects of lower renal function on cystatin C. No statistically significant differences in the levels of serum Cys-C were found among the tumor characteristics (all <i>P</i> > 0.05).