Programmed cell death (PCD), referring to apoptosis, autophagy and programmed necrosis, is proposed to be death of a cell in any pathological format, when mediated by an intracellular program. These three forms of PCD may jointly decide the fate of cells of malignant neoplasms; apoptosis and programmed necrosis invariably contribute to cell death, whereas autophagy can play either pro-survival or pro-death roles. Recent bulk of accumulating evidence has contributed to a wealth of knowledge facilitating better understanding of cancer initiation and progression with the three distinctive types of cell death. To be able to decipher PCD signalling pathways may aid development of new targeted anti-cancer therapeutic strategies. Thus in this review, we present a brief outline of apoptosis, autophagy and programmed necrosis pathways and apoptosis-related microRNA regulation, in cancer. Taken together, understanding PCD and the complex interplay between apoptosis, autophagy and programmed necrosis may ultimately allow scientists and clinicians to harness the three types of PCD for discovery of further novel drug targets, in the future cancer treatment.

As a conserved protein interaction module that recognizes and binds to acetylated lysine, bromodomain (BRD) contains a deep, largely hydrophobic acetyl lysine binding site. Proteins that share the feature of containing two BRDs and an extra-terminal domain belong to BET family, including BRD2, BRD3, BRD4 and BRDT. BET family proteins perform transcription regulatory function under normal conditions, while in cancer, they regulate transcription of several oncogenes, such as c-Myc and Bcl-2. Thus, targeting BET proteins may be a promising strategy, and intense interest of BET proteins has fueled the development of structure-based bromodomain inhibitors in cancer. In this review, we focus on summarizing several small-molecule BET inhibitors and their relevant anti-tumor mechanisms, which would provide a clue for exploiting new targeted BET inhibitors in the future cancer therapy.

The aim of this study was to investigate the effects of biochar amendment on soil aggregate formation and stability, and soil hydraulic properties. Biochar produced from dairy manure was added to two different soils (a silty clay and a sandy loam soil) at a ratio of 2% (w/w in dry weight basis). Incubation experiments were conducted within a 90-d period with the soils (the controls) and the soil/biochar mixtures. Compared with the controls, biochar addition significantly enhanced the formation of macroaggregates and slightly increased saturated hydraulic conductivities of the soils. Attributable to the soil structure change, saturated water contents increased and residual water contents decreased with the biochar amendment. These changes with biochar addition greatly affected the shape of soil water retention functions. For both the soil aggregate formation and the change of soil water retention curves, the sandy loam soil was more sensitive than the silty clay soil to the biochar application on all sampling days. The information from this study should be useful to better understand water processes in the soil with biochar application.

ULK1 is identified as a target in TNBC; thus a small-molecule agonist is discovered by targeting ULK1-modulated cell death, associated with autophagy and apoptosis.

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