MicroRNAs (miRNAs), small and non-coding endogenous RNAs ∼22 nucleotides (nt) in length, have been known to regulate approximately 30 % of human gene expression at the post-transcriptional and translational levels. Accumulating data have demonstrated that certain miRNAs could exert an oncogenic and/or tumor suppressive function and might play essential roles in the regulation of apoptosis and autophagy in cancer. In this review, we summarize that certain oncogenic and tumor suppressive miRNAs could modulate apoptotic pathways in different types of cancer. Subsequently, we demonstrate that other miRNAs might play regulatory roles in the autophagic pathways of cancer. A limited number of oncogenic/tumor suppressive miRNAs could regulate apoptosis and autophagy, respectively, and cooperatively. Taken together, these findings would provide a new clue to elucidate more apoptotic and/or autophagic mechanisms of miRNAs for designing potential novel therapeutic strategies in cancer.

Autophagy, the cell process of self-digestion, plays a pivotal role in maintaining energy homoeostasis and protein synthesis. When required, it causes degradation of long-lived proteins and damaged organelles, indicating that it may play a dual role in cancer, by both protecting against and promoting cell death. The autophagy-related gene (Atg) family, with more than 35 members, regulates multiple stages of the process. Serine/threonine protein kinase Atg1 in yeast, for example, can interact with other ATG gene products, functioning in autophagosome formation. One mammalian homologue of Atg1, UNC-51-like kinase 1 (ULK1) and its related complex ULK1-mAtg13-FIP200 can mediate autophagy under nutrient-deprived conditions, by protein-protein interactions and post-translational modifications. Although specific mechanisms of how ULK1 and its complex transduces upstream signals to the downstream central autophagy pathways is not fully understood, past studies have indicated that ULK1 can both suppress and promote tumour growth under different conditions. Here, we summarize some properties of ULK1 which can regulate autophagy in cancer, which may shed new light on future cancer therapy strategies, utilizing ULK1 as a potential new target.

Autophagy is a highly conserved lysosomal degradation process which can recycle unnecessary or dysfunctional cell organelles and proteins, thereby playing a crucial regulatory role in cell survival and maintenance. It has been widely accepted that autophagy regulates various pathological processes, among which cancer attracts much attention. Autophagy may either promote cancer cell survival by providing energy during unfavourable metabolic circumstance or can induce individual cancer cell death by preventing necrosis and increasing genetic instability. Thus, dual roles of autophagy may determine the destiny of cancer cells and make it an attractive target for small-molecule drug discovery. Collectively, key autophagy-related elements as potential targets, oncogenes mTORC1, class I PI3K and AKT, as well as tumour suppressor class III PI3K, Beclin-1 and p53, have been discussed. In addition, some small molecule drugs, such as rapamycin and its derivatives, rottlerin, PP242 and AZD8055 (targeting PI3K/AKT/mTORC1), spautin-1, and tamoxifen, as well as oridonin and metformin (targeting p53), can modulate autophagic pathways in different types of cancer. All these data will shed new light on targeting the autophagic process for cancer therapy, using small-molecule compounds, to fight cancer in the near future.