OBJECTIVE:To discuss the interactions between tetracyclines(oxytetracycline,methacycline,tetracydine,and doxycycline)and human serum albumin(HSA).METHODS:The binding constants and the number of biding sites of tetracyclines with human serum albumin(HSA)at various temperatures were studied by using UV-visible absorption spectrum and spectrofluorimetry,and the enthalpy change(?H)entropy change(?S)were computed.According to the Frster nonradiative energy transfer theory,the critical distances R0 between donators and acceptors were derived.RESULTS:The thermodynamic parameters were as follows:?H0;R0:oxytetracycline:(1.82 nm),and methacycline(2.31 nm),tetracydine(2.98 nm),doxycycline(2.26 nm).CONCLUSION:Tetracyclines can all cause HSA's fluorescence quenching.The quenching mechanism is static quenching.The main acting force between them is electrostatic attraction.

Metabolic reprogramming is a hallmark of cancer, including lung cancer. However, the exact underlying mechanism and therapeutic potential are largely unknown. Here we report that protein arginine methyltransferase 6 (PRMT6) is highly expressed in lung cancer and is required for cell metabolism, tumorigenicity, and cisplatin response of lung cancer. PRMT6 regulated the oxidative pentose phosphate pathway (PPP) flux and glycolysis pathway in human lung cancer by increasing the activity of 6-phospho-gluconate dehydrogenase (6PGD) and α-enolase (ENO1). Furthermore, PRMT6 methylated R324 of 6PGD to enhancing its activity; while methylation at R9 and R372 of ENO1 promotes formation of active ENO1 dimers and 2-phosphoglycerate (2-PG) binding to ENO1, respectively. Lastly, targeting PRMT6 blocked the oxidative PPP flux, glycolysis pathway, and tumor growth, as well as enhanced the anti-tumor effects of cisplatin in lung cancer. Together, this study demonstrates that PRMT6 acts as a post-translational modification (PTM) regulator of glucose metabolism, which leads to the pathogenesis of lung cancer. It was proven that the PRMT6-6PGD/ENO1 regulatory axis is an important determinant of carcinogenesis and may become a promising cancer therapeutic strategy.