ABSTRACT
A series of partially fused N-doped nanographenes (2-4) are synthesized via the oxidative cyclodehydrogenation of oligoaryl-substituted dibenzo[e,l]pyrene (1), and five, six, and seven new C-C bonds are formed, respectively, implying stepwise C-C bond fusion and extended π-conjugation. Single-crystal X-ray diffraction analysis of compound 4 a revealed that the presence of sterically demanding groups hindered the formation of planar and fully fused nanographene in the oxidative cyclodehydrogenation reaction step. Optical study of compounds 2 to 4 showed that extended π-conjugation leads to a regular stepwise bathochromic shift in the absorption and emission spectra. Furthermore, the HOMO-LUMO gaps of these compounds exhibit a decrease as C-C bond formation proceeds. Thus, the optoelectronic properties of nanographenes are highly dependent on the formation of new C-C bonds in the molecular skeleton.
ABSTRACT
Lung cancer is one of the most common malignancies worldwide, with high mortality and morbidity rates. O2â(2,4âdinitrophenyl)1â[(4ethoxycarbonyl)piperazin1yl]diazen1ium1,2diolate (JSK) is a potent anticancer agent that acts against a subset of human nonsmall cell lung cancer (NSCLC) cell lines; however, the underlying mechanisms of JSK in NSCLC remain unclear. The present study aimed to evaluate the anticancer effect of JSK and investigate its underlying mechanisms in A549 and H460 cells. In the present study, A549 and H460 cells were treated with JSK, and then evaluated by cell viability assay, flow cytometry and western blot analysis. JSK markedly induced cell cycle arrest at the G2/M phase in a concentration and timedependent manner in both cell lines. This was associated with increased expression levels of p53, and the cell cycle inhibitors p21WAF1/CIP1 and p27KIP1, which, in turn, inhibited the expression of Cdc2, cyclin B1 and cyclindependent kinase 2. In addition, JSKinduced inhibition of proliferation was revealed to be partially modulated by the upregulation of p53 and p21WAF1, the ratio of Bax/Bcl2, and the activation of both the intrinsic and extrinsic apoptotic pathways in A549 and H460 cells. These results demonstrated that JSK could trigger cell cycle arrest at the G2/M phase and apoptosis in A549 and H460 cells, which was likely mediated via the p53/p21WAF1/CIP1 and p27KIP1 pathways. Overall, the results indicated that JSK may be used as an anticancer agent for the treatment of NSCLC.