Apoptosis and autophagy in granulosa cells (GCs) are highly related to follicular development and atresia. LncRNA MEG3, miR-23a, and apoptosis signal-regulating kinase 1 (ASK-1) have also been reported to be associated with apoptosis and autophagy. However, their relationship to follicular development and the extent to which follicle stimulating hormone (FSH) or luteinizing hormone (LH) can regulate this process remains unknown in yak GCs. Here, the effect of LncRNA MEG3 / miR-23a on apoptosis and autophagy via ASK1 (Apoptosis signal-regulating kinase 1) / JNK (c-Jun N-terminal kinase) in yak GCs were studied. Overexpressing LncRNA MEG3 reduced miR-23a levels and p-967 protein expression, but enhanced ASK1 and JNK mRNA levels as well as t-ASK1, p-845, t-JNK, and p-JNK proteins levels, and promoted apoptosis while attenuating autophagy. Then, the interaction between LncRNA MEG and miR-23a and both miR-23a and ASK1 via dual-luciferase reporter assay was also confirmed. The relationship between LncRNA MEG3 and miR-23a was observed as a negative feedback regulation for ASK1/JNK axis via pcDNA3.1-MEG3 or miR-23a transfection which mimicked alone or in co-transfection. In addition, FSH (10 μg/mL) or LH (100 μg/mL) ability to reverse the effects of LncRNA MEG3 on miR-23a levels and ASK1/JNK axis-mediated apoptosis and autophagy was verified in yak GCs. This is significantly beneficial for decreasing abnormal follicular atresia.