miR-6553-3p regulates proliferation and differentiation of chicken myoblasts by targeting FAIM through the PI3K/AKT signaling pathway

Postnatal skeletal muscle growth in poultry relies on the precise orchestration of skeletal muscle satellite cell (SMSC) fate, yet the regulatory non-coding RNA networks governing this process remain partially veiled. Integrating small RNA sequencing with developmental expression profiling, we identified miR-6553-3p as a key differentially expressed regulator. Functional assays showed that miR-6553-3p markedly reduced SMSC proliferation while promoting myogenic differentiation. Specifically, miR-6553-3p significantly suppressed PAX7 expression at both the mRNA and protein levels, while simultaneously upregulating the mRNA and protein levels of MYOG and MYH1. Mechanistically, dual-luciferase assays confirmed that miR-6553-3p directly targeted Fas Apoptotic Inhibitory Molecule (FAIM). As an indispensable regulator of cellular homeostasis and cell fate decisions, FAIM is known to modulate key signaling cascades such as PI3K/AKT. In this study, we showed that FAIM normally sustained the proliferative pool of SMSCs; however, its repression by miR-6553-3p effectively attenuated AKT phosphorylation, linking this miRNA specifically to the PI3K/AKT pathway. By characterizing the miR-6553-3p–FAIM–AKT axis, our findings provide a molecular basis for fine-tuning muscle development and enhancing production traits during the critical early post-hatch window in the poultry industry.