Polycystic ovary syndrome (PCOS) is the leading cause of anovulation-associated infertility, accounting for 90-95% of all cases worldwide. Degenerative alterations in granulosa cell morphology and function are well documented in PCOS ovaries, particularly those which are anovulatory. These changes in PCOS granulosa cells play a key role in the development of infertility and are characterised by increased pyknotic appearance, reduced cell number and overall loss of granulosa cell layer integrity. Previous research has linked the mammalian target of rapamycin complex 1 (mTORC1) signalling pathway to poor ovulatory response in PCOS women. However, the exact mechanism through which the mTORC1 pathway contributes to infertility in PCOS remains unclear. In this study we examined how mTORC1 causes infertility in PCOS by pharmacological suppression of mTOR signalling in the granulosa cell line COV434. To confirm that mTORC1 signalling was decreased with pharmacological inhibition, we performed western blot analysis for pS6, a downstream effector and marker of mTORC1 activity. Western blot analysis revealed that pS6/mTORC1 activity was decreased in COV434 treated cells. To determine the effect of decreased mTORC1 signalling on COV434 cell function we performed viability and clonogenic assays, which reported reduced cell viability and colony forming ability with suppression of mTORC1. Collectively, these results suggest that the mTORC1 signalling pathway causes granulosa cell dysfunction in PCOS and thereby likely induces infertility.