Objectives Autophagy is the catabolic process that facilitates the degradation of proteins and organelles into recyclable nutrients for use by the cell. This article will review current literature to support the hypothesis that autophagy is pivotal in cancer progression and survival and provides some rationale behind the notion that autophagy can be a target for future cancer therapy. Key findings For the most part, autophagy is pro-cancerous in that it enables the affected cell to meet its nutritional requirements in hypoxic and cytotoxic environments (mainly due to chemotherapy), thus facilitating continued growth and proliferation of tumour cells. As such, it is reasonable to perceive autophagy as a mechanistic target for cancer therapy. However, the challenge to date has been the complexity of the mechanisms involved and the identification of key regulators of autophagy. This has been further complicated by the inherent variation between different cancer cell lines. Summary Better understanding of the role and mechanisms of autophagy in cancer, with a prelude to ways of exploiting this knowledge, may lead to better chemotherapeutic management of patients suffering from this currently incurable disease.

Objectives Autophagy facilitates the degradation of proteins or organelles into recyclable molecules, which are released into the cell to foster cell survival under energetic stress. Furthermore, autophagy has been associated with cancer cell survival and chemoresistance, and as such, it is an area of increasing interest. As autophagic activity and its regulation are related to metabolism and energy stress, it is critical to elucidate the exact molecular mechanisms that drive it. Key findings Cancer is recognised to have specific metabolic changes, which include the switch from oxidative phosphorylation to glycolysis. Although the exact rationale is yet to be determined, it is proposed to limit hypoxic stress and generate substrates for biosynthesis. The various forms of energetic stress including hypoxia, glucose and amino acid deprivation have been reviewed in relation to their effect on autophagy and certain key molecules identified to date. These key molecules, which include AMP-activated protein kinase, mammalian target of rapamycin complex 1, adenosine triphosphate and reactive oxygen species, are all implicated as key stimuli of autophagic activity, as will be discussed in this review. Summary These findings indicate that autophagic regulation could be a means to better cancer treatment.