Search

Background and aims: Increased nitrogen (N) deposition may exacerbate soil phosphorus (P) deficiency, which alters soil greenhouse gas (GHG) emissions by changing soil properties and understory vegetation in subtropical forests. However, the effects of N addition, P addition, and understory vegetation interactions on soil carbon dioxide (CO2) and nitrous oxide (N2O) emissions in forest ecosystems and their underlying mechanisms remain unclear. Methods: We conducted a continuous N and P addition experiment in a subtropical Chinese fir plantation. The effects of N and P addition on soil CO2 and N2O emissions with different understory vegetation were examined using a structural equation model. Results: The addition of N and P did not directly affect soil CO2 emission of the understory, which was affected by understory species (F = 2.86; p = 0.05). N indirectly and positively affects soil CO2 emission through plant elements, and directly affect N2O emission of understory soil. Compared with CK, the addition of N2 promoted the N2O cumulative emission by 74.3%. N has a direct positive effect on soil N2O emissions, while P addition indirectly exerts a negative influence on N2O emissions through its impact on soil properties. Plant elements and soil properties were explained in 26.3% of soil CO2 emissions, of which 17.6% and 16.0% variations were explained by plant elements and soil properties, respectively. Leaf total N was the most important factor for predicting CO2 emissions. Conclusions: Our results suggested that soil CO2 emission was more dependent on plant elements, and soil N2O emission was directly dependent on N addition rather than plant elements. Thus, different patterns of soil GHG emissions and associated controls following N and P addition provided novel insights into predicting the effects of understory vegetation on climate change mitigation outcomes. [ABSTRACT FROM AUTHOR]

As a newly identified type of programmed cell death, cuproptosis may have an impact on cancer development, including clear cell renal cell carcinoma (ccRCC). Herein, we first noticed that the expression levels of cuproptosis regulators exhibited a tight correlation with the clinicopathological characteristics of ccRCC. The cuproptosis-sensitive sub-type (CSS), classified via consensus clustering analysis, harbored a higher overall survival rate compared to the cuproptosis-resistant sub-type (CRS), which may have resulted from the differential infiltration of immune cells. FDX1, the cuproptosis master regulator, was experimentally determined as a tumor suppressor in ccRCC cells by suppressing the cell growth and cell invasion of ACHN and OSRC-2 cells in a cuproptosis-dependent and -independent manner. The results from IHC staining also demonstrated that FDX1 expression was negatively correlated with ccRCC tumor initiation and progression. Furthermore, we identified the miR-21-5p/FDX1 axis in ccRCC and experimentally verified that miR-21-5p directly binds the 3′-UTR of FDX1 to mediate its degradation. Consequently, a miR-21-5p inhibitor suppressed the cell growth and cell invasion of ACHN and OSRC-2 cells, which could be compensated by FDX1 knockdown, reinforcing the functional linkage between miR-21-5p and FDX1 in ccRCC. Finally, we evaluated the ccRCC tumor microenvironment under the miR-21-5p/FDX1 axis and noted that this axis was strongly associated with the infiltration of immune cells such as CD4+ T cells, Treg cells, and macrophages, suggesting that this signaling axis may alter microenvironmental components to drive ccRCC progression. Overall, this study constructed the miR-21-5p/FDX1 axis in ccRCC and analyzed its potential impact on the tumor microenvironment, providing valuable insights to improve current ccRCC management. [ABSTRACT FROM AUTHOR]