This study aimed to evaluate the involvement of miR‐125b and its interrelationship with follicle‐stimulating hormone (FSH) in the control of basic ovarian granulosa cell functions. The effect of miR‐125b mimics on basic functions of porcine ovarian granulosa cells cultured with and without FSH, and the effect of FSH on the expression of endogenous miR‐125b was examined. Expression levels of miR‐125b, viability, proliferation (accumulation of PCNA and cyclin B1), apoptosis (accumulation of bax and caspase 3), the accumulation of FSH receptors (FSHR), steroid hormones, insulin‐like growth factor I (IGF‐I), oxytocin, and prostaglandin E2 release were analysed by reverse transcription‐quantitative polymerase chain reaction, Trypan blue exclusion test, quantitative immunocytochemistry, and ELISA. Transfection of cells with miR‐125b mimics inhibited cell viability, proliferation, apoptosis, the occurrence of FSHR, progesterone, testosterone, estradiol, and oxytocin release but stimulated prostaglandin E2 output. FSH promoted cell viability, proliferation, steroid hormones, IGF‐I, oxytocin, and prostaglandin E2 output and reduced the expression of miR‐125b and apoptosis. Furthermore, miR‐125b mimics supported the effect of FSH on the release of estradiol, IGF‐I, and prostaglandin E2, and inverted FSH influence on cell viability, proliferation, apoptosis, progesterone, and testosterone output. FSH supported both inhibitory and stimulatory action of miR‐125b on ovarian cell functions. Present observations indicate that: miR‐125b can be involved in the control of basic ovarian functions and that miR‐125b and FSH are antagonists in their actions on ovarian cell functions. The ability of FSH to reduce miR‐125b expression and the ability of miR‐125b mimics to decrease the occurrence of FSHR and to modify FSH effects indicate the existence of the self‐inhibiting FSH‐miR‐125b axis and that miR‐125b can mediate the actions of FSH on ovarian cells.