A high spatial resolution carbon dioxide (CO2) emission map of China is proving to be essential for China's carbon cycle research and carbon reduction strategies given the current low quality of CO2 emission data and the inconsistencies in data quality between different regions. Ten km resolution CO2 emission gridded data has been built up for China based on point emission sources and other supporting data. The predominance of emissions from industrial point sources (84% of total emissions) in China supports the use of bottom-up methodology. The resultant emission map is informative and proved to be more spatially accurate than the EDGAR data. Spatial distribution of CO2 emissions in China is highly unbalanced and has positive spatial autocorrelation. The spatial pattern is mainly influenced by key cities and key regions, i.e., the Jing-Jin-Ji region, the Yangtze River delta region, and the Pearl River delta region. The emission map indicated that the supervision of 1% of total land could enable the management of about 70% of emissions in China.
Abnormal lipid metabolism has been commonly observed in various human cancers, including colorectal cancer (CRC). The mitochondrial citrate carrier SLC25A1 (also known as mitochondrial citrate/isocitrate carrier, CIC), has been shown to play an important role in lipid metabolism regulation. Our bioinformatics analysis indicated that SLC25A1 was markedly upregulated in CRC. However, the role of SLC25A1 in the pathogenesis and aberrant lipid metabolism in CRC remain unexplored. Here, we found that SLC25A1 expression was significantly increased in tumor samples of CRC as compared with paired normal samples, which is associated with poor survival in patients with CRC. Knockdown of SLC25A1 significantly inhibited the growth of CRC cells by suppressing the progression of the G1/S cell cycle and inducing cell apoptosis both in vitro and in vivo, whereas SLC25A1 overexpression suppressed the malignant phenotype. Additionally, we demonstrated that SLC25A1 reprogrammed energy metabolism to promote CRC progression through two mechanisms. Under normal conditions, SLC25A1 increased de novo lipid synthesis to promote CRC growth. During metabolic stress, SLC25A1 increased oxidative phosphorylation (OXPHOS) to protect protects CRC cells from energy stress-induced cell apoptosis. Collectively, SLC25A1 plays a pivotal role in the promotion of CRC growth and survival by reprogramming energy metabolism. It could be exploited as a novel diagnostic marker and therapeutic target in CRC.
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