Apigenin is a common dietary flavonoid that is abundantly present in many fruits, vegetables and Chinese medicinal herbs and serves multiple physiological functions, such as strong anti-inflammatory, antioxidant, antibacterial and antiviral activities and blood pressure reduction. Therefore, apigenin has been used as a traditional medicine for centuries. Recently, apigenin has been widely investigated for its anti-cancer activities and low toxicity. Apigenin was reported to suppress various human cancers in vitro and in vivo by multiple biological effects, such as triggering cell apoptosis and autophagy, inducing cell cycle arrest, suppressing cell migration and invasion, and stimulating an immune response. In this review, we focus on the most recent advances in the anti-cancer effects of apigenin and their underlying mechanisms, and we summarize the signaling pathways modulated by apigenin, including the PI3K/AKT, MAPK/ERK, JAK/STAT, NF-κB and Wnt/β-catenin pathways. We also discuss combinatorial strategies to enhance the anti-cancer effect of apigenin on various cancers and its use as an adjuvant chemotherapeutic agent to overcome cancer drug resistance or to alleviate other adverse effects of chemotherapy. The functions of apigenin against cancer stem cells are also summarized and discussed. These data demonstrate that apigenin is a promising reagent for cancer therapy. Apigenin appears to have the potential to be developed either as a dietary supplement or as an adjuvant chemotherapeutic agent for cancer therapy.

Targeting the αv integrin-TGF-β axis improves natural killer cell function against glioblastoma stem cells Running title-GBM induce NK cell dysfunction via integrin-TGF- axis

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Cell migration is an integral part of re-epithelialization during skin wound healing, a complex process involving molecular controls that are still largely unknown. Here we identify a novel role for Tcf3, an essential transcription factor regulating embryonic and adult skin stem cell functions, as a key effector of epidermal wound repair. We show that Tcf3 is upregulated in skin wounds and that Tcf3 overexpression accelerates keratinocyte migration and skin wound healing. We also identify Stat3 as an upstream regulator of Tcf3. We show that the pro-migration effects of Tcf3 are non-cell autonomous and occur independently of its ability to interact with β-catenin. Finally, we identify lipocalin-2 as the key secreted factor downstream of Tcf3 that promotes cell migration in vitro and wound healing in vivo. Our findings provide new insights into the molecular controls of wound-associated cell migration and identify potential therapeutic targets for the treatment of defective wound repair.

Precipitation alteration and nitrogen (N) deposition caused by anthropogenic activities could profoundly affect the structure and functioning of plant communities in arid ecosystems. However, the plant community impacts conferred by large temporal changes in precipitation, especially with a concurrent increase in N deposition, remain unclear. To address this uncertainty, from 2016 to 2017, an in situ field experiment was conducted to examine the effects of five precipitation levels, two N levels and their interaction on the plant community function and composition in a desert steppe in northern China. Above‐ground net primary production (ANPP) and plant community‐weighted mean (CWM) height significantly increased with increasing precipitation, and both were well fitted with a positive linear model, but with a higher slope under N addition. The ANPP increase was primarily driven by the increase in Artemisia capillaris, a companion forb sensitive to precipitation variation. The plant community composition shifted with precipitation enhancement—from a community dominated by Stipa tianschanica, a perennial grass, to a community dominated by Artemisia capillaris. Synthesis. The findings imply that the ecosystem sensitivity to future changes in precipitation variability will be mediated by two potential mechanisms: concurrent N deposition and plant community‐level change. It is suggested that we should consider the vegetation compositional shift and multiple resource colimitation in assessing the sensitivity of terrestrial ecosystems to climate change.