Purpose Workplace bullying is a common negative event suffered by employees in the workplace. The harm it brings to the organization has become the focus of the field of organizational behavior. The purpose of this study was to explore whether workplace bullying has an impact on employee knowledge hiding and to discover the underlying mechanism between the two. Design/methodology/approach Based on the conservation of resource theory and the cognitive-affective personality system theory, this paper surveys 327R&D employees of Chinese technological corporations at two time points and explores the relationship between workplace bullying and knowledge hiding as well as the underlying mechanism. This study used confirmatory factor analysis, bootstrapping method and structural equation model to validate the research hypothesis. Findings The results show that workplace bullying positively correlates with knowledge hiding; emotional exhaustion and organizational identification play a mediation role between workplace bullying and knowledge hiding, and both variables play a chain mediation role in that relationship; and forgiveness climate moderates the positive impact of workplace bullying on emotional exhaustion, further moderating the chain mediation role of emotional exhaustion and organizational identification. Originality/value The findings of this study can not only complement the existing researches on the influence of negative workplace events on employees’ knowledge hiding behaviors but also strengthen scholars’ attention and understanding of the internal mechanism between workplace bullying and knowledge hiding.

Angiogenesis is crucial for cancer initiation, development and metastasis. Identifying natural botanicals targeting angiogenesis has been paid much attention for drug discovery in recent years, with the advantage of increased safety. Isoliquiritigenin (ISL) is a dietary chalcone-type flavonoid with various anti-cancer activities. However, little is known about the anti-angiogenic activity of isoliquiritigenin and its underlying mechanisms. Herein, we found that ISL significantly inhibited the VEGF-induced proliferation of human umbilical vein endothelial cells (HUVECs) at non-toxic concentration. A series of angiogenesis processes including tube formation, invasion and migration abilities of HUVECs were also interrupted by ISL in vitro. Furthermore, ISL suppressed sprout formation from VEGF-treated aortic rings in an ex-vivo model. Molecular mechanisms study demonstrated that ISL could significantly inhibit VEGF expression in breast cancer cells via promoting HIF-1α (Hypoxia inducible factor-1α) proteasome degradation and directly interacted with VEGFR-2 to block its kinase activity. In vivo studies further showed that ISL administration could inhibit breast cancer growth and neoangiogenesis accompanying with suppressed VEGF/VEGFR-2 signaling, elevated apoptosis ratio and little toxicity effects. Molecular docking simulation indicated that ISL could stably form hydrogen bonds and aromatic interactions within the ATP-binding region of VEGFR-2. Taken together, our study shed light on the potential application of ISL as a novel natural inhibitor for cancer angiogenesis via the VEGF/VEGFR-2 pathway. Future studies of ISL for chemoprevention or chemosensitization against breast cancer are thus warranted.

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The authors' findings support the inclusion of walking exercise into the multimodal approaches to managing sleep in people with cancer. Healthcare providers must convey the benefits of walking exercise to individuals with cancer who are suffering from sleep problems.