[Spatial and temporal variation in normalized difference vegetation index of vegetation in Liaoning Province from the perspective of ecogeographic zoning]. / 生态地理分区视角下的辽宁省植被归一化植被指数的时空变化.

Normalized difference vegetation index (NDVI) is an important indicator reflecting vegetation cover and growth status. It is of significance for regional ecological conservation and natural resource management to investigate its spatial and temporal variation trends and response to ecological factors. We divided Liaoning Province into three ecological geographical regions, including northwest agro-pastoral zone, central agricultural zone, and eastern agroforestry zone. Based on remote sensing, vegetation, climate, topography and human activities, we used trend analysis and geographic probe model to examine the spatial and temporal trends of NDVI in Liaoning Province, and analyzed the intensity and interaction mechanism of each driver on the spatial distribution pattern of NDVI. The results showed that the annual average NDVI in Liaoning Province from 2001 to 2020 was 0-0.92, showing a distribution pattern of high in the east and low in the west, high in the inland and low in the coastal land. The overall trend of vegetation cover was increasing, and the NDVI increasing areas were mainly concentrated in the northwest agro-pastoral zone and the eastern agroforestry zone, the NDVI reduction areas were mainly concentrated at the border between the central agricultural zone and the eastern agroforestry zone, as well as in the coastal area of the eastern agroforestry zone. The annual average NDVI change varied among the three ecological-geographic zones. The NDVI of the northwest agro-pastoral zone from 2001 to 2020 were generally low, but showed a fluctuating trend of slow increase. The NDVI of the eastern agroforestry zone was high overall, and the interannual variation of NDVI was generally stable. The distribution of high and low NDVI in the central agricultural zone was staggered, and the interannual variation of NDVI showed a decreasing trend. Natural factors were the key drivers of NDVI changes in the three ecogeographic zones, with cumulative temperature and precipitation having the greatest influence. The interactions between the factors were all mutually and nonlinearly enhanced.

Enhancing tumor chemotherapy and overcoming drug resistance through autophagy-mediated intracellular dissolution of zinc oxide nanoparticles.

Autophagy may represent a common cellular response to nanomaterials. In the present study, it was demonstrated that zinc oxide nanoparticle (ZON)-elicited autophagy contributes to tumor cell killing by accelerating the intracellular dissolution of ZONs and reactive oxygen species (ROS) generation. In particular, ZONs could promote Atg5-regulated autophagy flux without the impairment of autophagosome-lysosome fusion, which is responsible for ZON-elicited cell death in cancer cells. On the other hand, a further study revealed that a significant free zinc ion release in lysosomal acid compartments and sequential ROS generation in cells treated with ZONs were also associated with tumor cytotoxicity. Intriguingly, the colocalization between FITC-labeled ZONs and autophagic vacuoles indicates that the intracellular fate of ZONs is associated with autophagy. Moreover, the chemical or genetic inhibition of autophagy significantly reduced the level of intracellular zinc ion release and ROS generation separately, demonstrating that ZON-induced autophagy contributed toward cancer cell death by accelerating zinc ion release and sequentially increasing intracellular ROS generation. The modulation of autophagy holds great promise for improving the efficacy of tumor chemotherapy. Herein, ZONs were verified to enhance chemotherapy in both normal and drug-resistant cancer cells via synergistic autophagy elicitation. Further, this elicitation resulted in tremendous zinc ion release and ROS generation, which accounted for enhancing the tumor chemotherapy and overcoming drug resistance. No obvious changes in the expression level of P-gp proteins or the amount of doxorubicin uptake induced by ZONs in MCF-7/ADR cells also indicated that the increased zinc ion release and ROS generation via synergistic autophagy induction were responsible for overcoming the drug resistance. Finally, in vivo experiments involving animal models of 4T1 tumor cells revealed that the antitumor therapeutic effect of a combinatory administration obviously outperformed those of ZONs or free doxorubicin treatment alone at the same dose, which could be attenuated by the autophagy inhibitor wortmannin or ion-chelating agent EDTA. Taken together, our results reveal the mechanism wherein the autophagy induction by ZONs potentiates cancer cell death and a novel biological application for ZONs in adjunct chemotherapy in which autophagy reinforces zinc ion release and ROS generation.

Brucine Suppresses Vasculogenic Mimicry in Human Triple-Negative Breast Cancer Cell Line MDA-MB-231.

Vasculogenic mimicry (VM) with the pattern of endothelial independent tubular structure formation lined by aggressive tumor cells mimics regular tumor blood vessels to ensure robust blood supply and correlates with the proliferation, invasion, metastasis, and poor prognosis of malignant tumors, which was demonstrated to be a major obstacle for resistance to antiangiogenesis therapy. Therefore, it is urgent to discover methods to abrogate the VM formation of tumors, which possesses important practical significance for improving tumor therapy. Brucine is a traditional medicinal herb extracted from seeds of Strychnos nux-vomica L. (Loganiaceae) exhibiting antitumor activity in a variety of cancer models. In the present study, the effect of brucine on vasculogenic mimicry and the related mechanism are to be investigated. We demonstrated that, in a triple-negative breast cancer cell line MDA-MB-231, brucine induced a dose-dependent inhibitory effect on cell proliferation along with apoptosis induction at higher concentrations. The further study showed that brucine inhibited cell migration and invasion with a dose-dependent manner. Our results for the first time indicated that brucine could disrupt F-actin cytoskeleton and microtubule structure, thereby impairing hallmarks of aggressive tumors, like migration, invasion, and holding a possibility of suppressing vasculogenic mimicry. Hence, the inhibitory effect of brucine on vasculogenic mimicry was further verified. The results illustrated that brucine significantly suppressed vasculogenic mimicry tube formation with a dose-dependent effect indicated by the change of the number of tubules, intersections, and mean length of tubules. The in-depth molecular mechanism of vasculogenic mimicry suppression induced by brucine was finally suggested. It was demonstrated that brucine inhibited vasculogenic mimicry which might be through the downregulation of erythropoietin-producing hepatocellular carcinoma-A2 and matrix metalloproteinase-2 and metalloproteinase-9.