Search

Against the background of global warming, trees in high-latitude and high-altitude areas are more sensitive to rapid warming. Revealing the response patterns of trees at different altitudes to rapid warming in typical alpine mountain environments can help to predict the future distribution of forests in the region and the associated changes in the timberline. This study used tree-ring width data (band sampling) from Dahurian larch (Larix gmelinii Rupr.) along an altitudinal gradient (970–1409 m) on Oakley Mountain to establish 10 chronologies and to analyze the growth–climate response of larch to warming and altitudinal changes along a gradient. The results showed that before rapid warming, larch growth was strongly influenced mainly by precipitation in July–August, while after warming, the growth was controlled mainly by precipitation (snowfall) in winter (October–April) and showed a significant positive correlation with the SPEI in winter and a negative correlation with temperature in February–April (early spring). This indicates that the rapid warming event led to a drastic change in the water heat balance during the pre-growth period of the trees in the study area, which shifted the tree growth from being restricted by drought in the growing season before warming to being restricted by winter drought (i.e., the lagged effect of snowfall in the pre-growing season) after warming and that the trees at low altitudes suffered from more severe winter drought. In the future, as the global climate warms further, the growth of mountain larch at low altitudes (below 1200 m) will continue to decrease, and the coupling of winter snowfall and seasonal (February–April) warming will increase the upper altitude limit at which winter drought occurs for larch in the study area; additionally, larch at higher altitudes will be able to cope with this ecological process better. [ABSTRACT FROM AUTHOR]

Objective: Most patients with osteosarcoma (OS) have an extremely poor prognosis. The primary purpose of this investigation was to explore the biological effect of Lnc-CLSTN2-1:1 on OS and the potential processes involved. Materials and procedures: We selected differentially overexpressed Lnc-CLSTN2-1:1 from our laboratory's existing RNA sequence analysis data (fibroblast osteoblast (hFOB 1.19) and three osteosarcoma cell lines (HOS, MG63, and U2OS) as the research object. Next, we detected Lnc-CLSTN2-1:1 in the osteosarcoma HOS cell line and fibroblast cells using qRT-PCR. We evaluated cell proliferation ability using EdU incorporation test, CCK-8 test, and cell clone formation; cell invasion and migration were assessed using the Transwell test, while flow cytometry examined cell cycle, apoptosis, and reactive oxygen species (ROS); Subsequently, the activity changes of selenase (GPx) glutathione peroxidase and (TrxR) thioredoxin reductase were detected. In addition, changes in related proteins were analyzed through Western blotting. Results: The expression of Lnc-CLSTN2-1:1 in osteosarcoma cells was significantly increased. The proliferation, invasion, and migration of osteosarcoma cells were significantly inhibited by knockdown of the expression of Lnc-CLSTN2-1:1, and the cell cycle-related signaling pathway PI3K/AKT/GSK-3β/cycinD1 was also inhibited. However, insulin-like growth factor-1 (igf-1) could reverse this process. In addition, we examined the activity of two selenophenases (TrxR and GPx) and the changes of ROS before and after Lnc-CLSTN2-1:1 knockdown. The results showed that both TrxR and GPx activities were reduced after Lnc-CLSTN2-1:1 knockdown, resulting in the inhibition of antioxidant stress levels, while intracellular ROS levels were high, which eventually caused killing effects on tumor cells due to the imbalance between oxidative stress and antioxidant stress. Conclusion: Our results showed that Lnc-CLSTN2-1:1 enhanced anti-oxidative stress TrxR and GPx selenoprotein activities through the PI3K/AKT signaling pathway while counteracting the loss of reactive oxygen species ROS produced by mitochondria to osteosarcoma cells, which protected osteosarcoma cells and thus promoted the proliferation and metastatic ability of OS., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)