〔Abstract〕 Cachexia is one of the serious complications in patients with end-stage cancer. Progressive depletion of skeletal muscle is an important feature of cachexia. Previous studies have found that excessive activation of autoph- agy accelerates skeletal muscle wasting in cachexia , and glutamine released from excessive catabolism of muscle tis- sue can trigger the autophagy . Mammalian target of rapamycin complex 1 ( mTORC1) and AMP-activated protein kinase (AMPK) signaling regulate autophagy genesis; moreover , glutamine regulates the mTORC1 and AMPK sig- naling pathways . Therefore , it is deduced that higher level of glutamine may result in abnormal autophagy by regu- lating mTORC1 and AMPK in cancer cachexia , which contributes to the development of skeletal muscle wasting. Here , this review discusses the following three perspectives : firstly , autophagy hyperactivation is involved in skele- tal muscle wasting in cancer cachexia. Secondly , how mTORC1 and AMPK signaling pathways regulate autophagy . Finally , glutamine is involved in skeletal muscle wasting in cancer cachexia by induced autophagy hyperactivation via regulating mTORC1 /AMPK signaling. Our study will provide a scientific basis for the development of potential therapeutic strategies .